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PubMed2000

Nonsurgical periodontal therapy.

The primary etiology of periodontal disease is bacterial infection. Bacteria exist as a biofilm (plaque) on the tooth and soft-tissue surfaces of the mouth. Biofilm is extremely resistant to antimicrobial activity. To effectively treat periodontal disease, the bacterial load must be reduced to allow healing of the inflamed tissues. Reduction of the bacterial load can be accomplished by surgical methods, nonsurgical methods, or a combination of the two. This article focuses on the nonsurgical treatment of periodontal disease. A thorough oral examination, which includes visual inspection and the use of a periodontal probe, is needed to determine the best therapy. Supragingival cleaning with power and hand scalers is the first step in the therapy process. The next step, subgingival scaling, is necessary to remove bacteria that are in direct contact with the periodontium. Effective subgingival plaque removal is time intensive and requires motivation, manual dexterity, and meticulous technique. Most veterinarians and veterinary technicians lack the training, instruments, and time to remove subgingival plaque effectively. To improve therapeutic results, adjunctive therapy in the form of oral systemic antibiotics or a locally applied doxycycline-containing polymer may be used. The success of periodontal therapy also is dependent on dental home care that takes place after professional treatment. The veterinarian and staff must be willing to educate and reinforce the dental home care efforts of the pet owner.

Animals↗

PubMed2004

In vitro combined effect of co-amoxiclav concentrations achievable in serum after a 2000/125 mg oral dose, and polymorphonuclear neutrophils against strains of Streptococcus pneumoniae exhibiting decreased susceptibility to amoxicillin.

The in vitro effect that the presence of components of non-specific immunity (serum plus polymorphonuclear neutrophils) has on the bactericidal activity of co-amoxiclav was explored against Streptococcus pneumoniae strains exhibiting an amoxicillin MIC > or =4 mg/L. Eight penicillin-resistant clinical isolates non-susceptible to co-amoxiclav with MICs of 4 (two strains), 8 (four strains) and 16 mg/L (two strains) were used. Values of MBC were identical to MIC values in all cases. Time-kill curves were performed with co-amoxiclav concentrations achievable in serum after a single oral dose administration of the new 2000/125 mg sustained-release formulation. Results were expressed as percentage of reduction of initial inocula after 3 h incubation. Control curves showed growth with no reduction of initial inocula. Against strains with MIC of 4 and 8 mg/L, the results obtained with the antibiotic alone or with the presence of factors of non-specific immunity were similar, with a weak combined effect due to the intrinsic activity of co-amoxiclav (reductions of initial inocula ranging from 70 to 99.16%). Against strains with MIC of 16 mg/L, the addition of PMN in the presence of serum increased the reduction of bacterial load provided by the aminopenicillin, even at sub-inhibitory concentrations (25.8% versus 51.1% at 0.5 x MIC concentration--8/0.5 mg/L). This combined activity against strains with an amoxicillin MIC of 16 mg/L which decreased the bacterial load may be important in preventing bacterial proliferation within the host and the transmission of resistant clones to others.

Administration, Oral↗

PubMed2006

Meningococcal disease deaths and the frequency of antibiotic administration delays.

OBJECTIVE: Meningococcal disease (MCD) remains a medical emergency and a frequent cause of death in previously healthy individuals. We aimed to determine the frequency and cause of delays in antibiotic administration in a cohort of deaths. METHODS: A retrospective chart review was undertaken on 140 hospitalised MCD deaths within New Zealand's serogroup B epidemic (1993-2004). RESULTS: Death after hospital presentation occurred rapidly (median 12 h) with 70% dying within 24 h. Delays of more than 2 h in time-to-antibiotic post hospital presentation occurred in 29%. The major contributors to these delays were the failure to include MCD within the differential diagnosis and prolonged assessment times. Multivariate logistic regression analysis, undertaken by combining study deaths which had meningococcal bacterial load results (n=9) with a survivor cohort (n=126) from a previous study, confirmed bacterial load as a major predictor of death (OR 7.5 per log10 cfu/mL increase; 95% CI 2.2-25.3; p=0.001). A non-significant increased risk of death per hour of antibiotic delay was seen (OR 1.18; 95% CI 0.90-1.55; p=0.22). CONCLUSIONS: Death from MCD occurred rapidly, with many patients not receiving antibiotics at the earliest opportunity. The introduction of recently developed rapid diagnostic markers into the identified delay-intervals could lead to a reduction in time-to-antibiotic and hopefully reduce case-fatality rates.

Adolescent↗

PubMed2004

Induction of persistent in vivo resistance to Mycobacterium avium infection in BALB/c mice injected with interleukin-18-secreting fibroblasts.

Interferon-gamma (IFN-gamma) is closely associated with the generation of cell-mediated immunity and resistance to intracellular parasites. Interleukin-18 (IL-18) is known to strongly induce IFN-gamma production by T cells and natural killer (NK) cells. To determine whether the paracrine secretion of IL-18 can efficiently stimulate the resistance to Mycobacterium avium complex (MAC) infection, 3T3 fibroblasts were stably transfected to secrete bioactive IL-18 and their effects on MAC infection were investigated in genetically susceptible BALB/c mice, compared with that of free recombinant IL-18. Immunization with IL-18-secreting fibroblasts (3T3/IL-18) during intranasal infection with MAC resulted in a significant decrease in bacterial load of lung during the entire 8-week observation period, while rIL-18 reduced the bacterial load at initial 1 week but not by 8 weeks postinfection. Immunization with the 3T3/IL-18 cells induced and maintained significantly higher levels of cytotoxic activity and nitric oxide production by lung cells than those of rIL-18 immunization. Furthermore, lung cells in mice injected with the 3T3/IL-18 cells showed persistent production of IFN-gamma throughout the 8-week period, suggesting that the 3T3/IL-18 cells induced the resistance to MAC infection via IFN-gamma production. This work suggests that IL-18-secreting fibroblasts may serve as a vehicle for paracrine secretion of IL-18 in immunotherapy of MAC infection.

3T3 Cells↗

PubMed2000

Induction of in vivo persistent anti-mycobacterial activity by interferon-gamma-secreting fibroblasts.

To determine whether the paracrine secretion of interferon-gamma (IFN-gamma) can efficiently stimulate the resistance to Mycobacterium avium complex (MAC) infection, 3T3 fibroblasts were stably transduced to secrete IFN-gamma (500 units/10(6) cells/48 h) and their effects on MAC infection were investigated in genetically susceptible BALB/c mice, compared with that of free recombinant IFN-gamma (rIFN-gamma). Immunization with IFN-gamma-secreting fibroblasts (3T3-IFN-gamma) during intranasal infection with MAC resulted in a significant decrease in bacterial load of lung during the entire 8-week observation period, while rIFN-gamma reduced the bacterial load at initial 1 week but not by 8 weeks postinfection. Furthermore, immunization with the 3T3-IFN-gamma cells induced and maintained significantly higher levels of cytotoxic activity and nitric oxide production by lung cells than those of rIFN-gamma immunization. This work suggest that IFN-gamma-secreting fibroblasts may serve as a vehicle for paracrine secretion of IFN-gamma in immunotherapy of MAC infection.

3T3 Cells↗

PubMed1999

Interleukin-12-secreting fibroblasts are more efficient than free recombinant interleukin-12 in inducing the persistent resistance to Mycobacterium avium complex infection.

To determine whether the paracrine secretion of interleukin-12 (IL-12) can efficiently stimulate the resistance to Mycobacterium avium complex (MAC) infection, 3T3 fibroblasts were stably transfected to secrete IL-12 (480 U/106 cells/48 hr) and their effect on MAC infection was investigated in genetically susceptible BALB/c mice, compared with that of free recombinant IL-12 (rIL-12). Injection with IL-12-secreting fibroblasts (3T3-IL-12) during intranasal infection with MAC resulted in a significant decrease in the bacterial load of the lung during the entire 10-week observation period, while rIL-12 reduced the bacterial load initially, at 2 weeks, but not by 10 weeks postinfection. Lung CD4+ T cells in mice injected with the 3T3-IL-12 cells showed a persistent T helper type 1 (Th1) response throughout the 10-week period. Furthermore, immunization with the 3T3-IL-12 cells induced and maintained significantly higher levels of cytotoxic activity and nitric oxide production by lung cells than did rIL-12 immunization. This work suggests that IL-12-secreting fibroblasts may serve as a vehicle for paracrine secretion of IL-12 for immunotherapy of MAC infection.

Animals↗

PubMed2000

CD8(+) T-cell priming against a nonsecreted Listeria monocytogenes antigen is independent of the antimicrobial activities of gamma interferon.

Sublethal infection of mice with recombinant Listeria monocytogenes expressing a model epitope in either secreted or nonsecreted form results in similar CD8(+) T-cell priming. Since nonsecreted bacterial proteins have no obvious access to the endogenous major histocompatibility complex (MHC) class I presentation pathway, presentation of these antigens requires destruction of the bacterium to reveal the nonsecreted molecules to an exogenous MHC class I presentation pathway. Gamma interferon (IFN-gamma), a cytokine made by multiple cell types in response to L. monocytogenes infection, could be required for exogenous presentation of nonsecreted bacterial antigens via its capacity to upregulate the expression of molecules involved in antigen presentation, its capacity to activate macrophages to kill bacteria to expose nonsecreted molecules or both. IFN-gamma knockout (KO) mice were used to address the requirement for IFN-gamma in CD8(+) T-cell priming against (i) a model exogenous antigen and (ii) secreted and nonsecreted L. monocytogenes antigens. We demonstrate that IFN-gamma KO mice are capable of cross-presenting the model exogenous antigen ovalbumin to prime CD8(+) T-cell responses that are only slightly weaker than that in wild-type (WT) mice. Despite their extreme susceptibility to primary L. monocytogenes infection, previously immunized and naive IFN-gamma KO mice were able to generate CD8(+) T-cell responses against both secreted and nonsecreted L. monocytogenes antigens which were similar to responses of WT mice. Interestingly, IFN-gamma KO mice were as capable as WT mice in mediating the characteristic drop in bacterial load in the liver at 4 h postinfection, although the IFN-gamma KO mice have exacerbated bacterial loads as early as 24 h postinfection. These results demonstrate that the regulatory functions of IFN-gamma are not required for priming of CD8(+) T cells by cross-presentation of a model exogenous antigen or in response to a nonsecreted L. monocytogenes antigen. In addition, the capacity of IFN-gamma to activate the microbicidal activities of macrophages is not required for the very early innate immune response to L. monocytogenes or priming of CD8(+) T cells against a nonsecreted bacterial antigen.

Animals↗

PubMed2004

The knockout of the lprG-Rv1410 operon produces strong attenuation of Mycobacterium tuberculosis.

P27 lipoprotein was previously described as an antigen in the Mycobacterium tuberculosis complex, encoded by the lprG gene, also named Rv1411 in the TubercuList (http://genolist.pasteur.fr/TubercuList) gene bank. It forms an operon with Rv1410 that encodes for an efflux pump, P55. A mutant of the H37Rv strain of M. tuberculosis not producing P27 (strain DeltaP27) was obtained by two-step mutagenesis using the counterselectable marker sacB and a thermosensitive origin of replication in the shuttle plasmid pPR27. By RT-PCR, we observed no lprG or Rv1410 mRNA in the DeltaP27 mutant strain compared with the wild type and complemented strains. Western blot experiments using anti-P27 polyclonal sera showed that the P27 protein was present both in the parental and in a complemented strain, in which the entire lprG-Rv1410 operon was reintroduced, but absent in the mutant strain. The three strains showed similar growth kinetics and characteristics in culture broth. To study the effect of the lprG mutation on M. tuberculosis virulence, BALB/c mice were inoculated to determine bacterial loads in spleens. At days 15 and 35 after infection, decreases of 1.5 and 2.5 logs in the bacterial load were found, respectively, in animals inoculated with the DeltaP27 mutant strain or with the wild type. This attenuation was reverted in the complemented strain. These results demonstrated that lprG gene is required for growth of M. tuberculosis in immunocompetent mice. The reversion of attenuation in the complemented strain indicates that the attenuated phenotype resulted from disruption of the lprG-Rv1410 operon.

Animals↗

PubMed2000

CpG oligodeoxynucleotides and interleukin-12 improve the efficacy of Mycobacterium bovis BCG vaccination in mice challenged with M. tuberculosis.

Mycobacterium bovis bacillus Calmette-Guérin (BCG) is the only vaccine approved for prevention of tuberculosis. It has been postulated that serial passage of BCG over the years may have resulted in attenuation of its effectiveness. Because interleukin-12 (IL-12) and oligodeoxynucleotides (ODN) containing cytidine phosphate guanosine (CpG) motifs have been shown to enhance Th1 responses in vivo, they were chosen as adjuvants to increase the effectiveness of BCG vaccination. In this report, mice were vaccinated with BCG with or without IL-12 or CpG ODN and then challenged 6 weeks later via the aerosol route with the Erdman strain of M. tuberculosis. Mice vaccinated with BCG alone showed a 1- to 2-log reduction in bacterial load compared with control mice that did not receive any vaccination prior to M. tuberculosis challenge. Moreover, the bacterial loads of mice vaccinated with BCG plus IL-12 or CpG ODN were a further two- to fivefold lower than those of mice vaccinated with BCG alone. As an immune correlate, the antigen-specific production IFN-gamma and mRNA expression in spleen cells prior to challenge were evaluated. Mice vaccinated with BCG plus IL-12 or CpG ODN showed enhanced production of IFN-gamma compared with mice vaccinated with BCG alone. Finally, granulomas in BCG-vaccinated mice were smaller and more lymphocyte rich than those in unvaccinated mice; however, the addition of IL-12 or CpG ODN to BCG vaccination did not alter granuloma formation or result in added pulmonary damage. These observations support a role for immune adjuvants given with BCG vaccination to enhance its biologic efficacy.

Adjuvants, Immunologic↗

PubMed2005

Evaluation of Helicobacter hepaticus bacterial shedding in fostered and sex-segregated C57BL/6 mice.

Neonatal fostering has been evaluated as a means of eliminating Helicobacter hepaticus infection in laboratory mouse colonies. The purpose of the present study was to evaluate cross-fostering of neonatal C57BL/6 pups from experimentally infected dams after male-absent parturition and to determine the effects of sex and housing strategy on H. hepaticus populations. Approximately 20 C57BL/6 mice (age, 1 to 4 days) were fostered daily. In all fostered mice, fecal samples collected at 21 and 42 days of age and cecal samples collected at 42 days of age tested negative for H. hepaticus by polymerase chain reaction analysis. Our results demonstrate that removal of the male prior to parturition extends the fostering period to yield Helicobacter-free mice. In a second experiment, the effects of time of infection, housing strategy, and sex on fecal H. hepaticus shedding and cecal colonization were evaluated. Neither time nor housing strategy affected bacterial shedding. In contrast, fecal and cecal bacterial loads were higher in male mice versus female mice. A novel predictive algorithm was developed to predict cecal bacterial colonization levels in light of fecal bacterial loads. Our findings likely will prove useful in Helicobacter eradication efforts and in studies designed to further elucidate the role of H. hepaticus in disease.

Algorithms↗

PubMed2004

Immunostimulatory CpG oligodeoxynucleotide confers protection in a murine model of infection with Burkholderia pseudomallei.

Although CpG oligodeoxynucleotides (CpG ODNs) are known to enhance resistance against infection in a number of animal models, little is known about the CpG-induced protection against acute fatal sepsis such as that associated with the highly virulent bacterium Burkholderia pseudomallei. We previously demonstrated in an in vitro study that immunostimulatory CpG ODN 1826 enhances phagocytosis of B. pseudomallei and induces nitric oxide synthase and nitric oxide production by mouse macrophages. In the present study, CpG ODN 1826 given intramuscularly to BALB/c mice 2 to 10 days prior to B. pseudomallei challenge conferred better than 90% protection. CpG ODN 1826 given 2 days before the bacterial challenge rapidly enhanced the innate immunity of these animals, judging from the elevated serum levels of interleukin-12 (IL-12)p70 and gamma interferon (IFN-gamma) over the baseline values. No bacteremia was detected on day 2 in 85 to 90% of the CpG-treated animals, whereas more than 80% of the untreated animals exhibited heavy bacterial loads. Although marked elevation of IFN-gamma was found consistently in the infected animals 2 days after the bacterial challenge, it was ameliorated by the CpG ODN 1826 pretreatment (P = 0.0002). Taken together, the kinetics of bacteremia and cytokine profiles presented are compatible with the possibility that protection by CpG ODN 1826 against acute fatal septicemic melioidosis in this animal model is associated with a reduction of bacterial load and interference with the potential detrimental effect of the robust production of proinflammatory cytokines associated with B. pseudomallei multiplication.

Adjuvants, Immunologic↗

PubMed2002

Model of differential susceptibility to mucosal Burkholderia pseudomallei infection.

Burkholderia pseudomallei is the causative agent of melioidosis, an infectious disease with protean clinical manifestations. The major route of infection is thought to be through subcutaneous inoculation of contaminated soil and water, although ingestion and inhalation of contaminated aerosols are also possible. This study examines infection through the intranasal route in a murine model to mimic infection through inhalation. Two strains of mice, C57BL/6 and BALB/c, exhibit differential susceptibilities to the infection, with the C57BL/6 mice being considerably more resistant. To examine host factors that could contribute to this difference, bacterial loads and cytokine profiles in the two strains of mice were compared. We found that infected BALB/c mice exhibited higher bacterial loads in the lung and spleen and that they produced significantly higher levels of gamma interferon (IFN-gamma) in the serum than C57BL/6 mice. Although tumor necrosis factor alpha and interleukin-1 could be detected in the nasal washes and sera of both strains of mice, the production in serum was transient and much lower than that of IFN-gamma. C57BL/6 mice also exhibited memory responses to bacteria upon reinfection, with the production of serum immunoglobulin G (IgG) and mucosal IgA antibodies. Thus, it is possible that the production of systemic and mucosal antibodies is important for protection against disease in C57BL/6 mice.

Administration, Intranasal↗

PubMed1982

An immunoperoxidase study of immunological factors in skin lesions across the spectrum of leprosy.

The immunoperoxidase technique was used to assess the quantity and situation of various immunological factors in 24 skin biopsies which represented the leprosy spectrum from TT to LL. The factors were immunoglobulins (IgG and IgM), complement components (C3, C3d and Clq), plasminogen, muramidase (lysozyme), C-reactive protein and alpha-1-antitrypsin. The results were compared with previous reports on the assessment of these factors in serum. The quantities of these factors in the lesions produced peaks at TT and LL, with a dip in the BT-BB region (C-reactive protein and alpha-1-antitrypsin excepted). The immunoglobulins, present mainly in plasma cells and lymphocytes, correlated in general with reports of serum levels. The complement components were present in appreciable amounts, though the serum levels are depressed; they were seen in young mononuclear cells with a low bacterial load. All factors produced an ascending gradient in active lesions from BT to BL or LL, which correlated with the bacterial load and its viability. In regression (studied only in LL) there was a decrease in all factors. In TT there was an increase in most factors which did not correlate with the antigen load, and which probably resulted in an excess of antibody over antigen. In active LL there is probably an antigen excess. The results suggest the possibility that there is a common defect from BT to LL, in which the generation of immunological factors within the lesion of immunological factors within the lesion is a secondary response to the antigenic load. In TT alone (a rare group) is there an enhanced immunological response unrelated to the antigen load. In support of this was the finding of Ia antigen only in TT lesions.

Complement System Proteins↗

PubMed2006

Differential clearance and immune responses to tick cell-derived versus macrophage culture-derived Ehrlichia chaffeensis in mice.

Human monocytic ehrlichiosis is caused by a tick-transmitted rickettsia, Ehrlichia chaffeensis. We recently reported that E. chaffeensis grown in tick cells expresses different proteins than bacteria grown in macrophages. Therefore, we tested the hypothesis that immune responses against E. chaffeensis would be different if the mice are challenged with bacteria grown in macrophages or tick cells. We assessed the E. chaffeensis clearance from the peritoneum, spleen, and liver by C57BL/6J mice using a TaqMan-based real-time reverse transcription-PCR assay. Macrophage-grown E. chaffeensis was cleared in 2 weeks from the peritoneum, whereas the pathogen from tick cells persisted for nine additional days and included three relapses of increasing bacterial load separated by three-day intervals. Tick cell-grown bacteria also persisted in the livers and spleens with higher bacterial loads compared to macrophage-grown bacteria and fluctuated over a period of 35 days. Three-day periodic cycles were detected in T-cell CD62L/CD44 ratios in the spleen and bone marrow in response to infections with both tick cell- and macrophage-grown bacteria and were accompanied by similar periodic cycles of spleen cell cytokine secretions and nitric oxide and interleukin-6 by peritoneal macrophages. The E. chaffeensis-specific immunoglobulin G response was considerably higher and steadily increased in mice infected with the tick cell-derived E. chaffeensis compared to DH82-grown bacteria. In addition, antigens detected by the immunoglobulins were significantly different between mice infected with the E. chaffeensis originating from tick cells or macrophages. The differences in the immune response to tick cell-grown bacteria compared to macrophage-grown bacteria reflected a delay in the shift of gene expression from the tick cell-specific Omp 14 gene to the macrophage-specific Omp 19 gene. These data suggest that the host response to E. chaffeensis depends on the source of the bacteria and that this experimental model requires the most natural inoculum possible to allow for a realistic understanding of host resistance.

Animals↗

PubMed1999

Attenuated host resistance against Mycobacterium bovis BCG infection in mice lacking osteopontin.

Expression of the cytokine osteopontin (OPN) is elevated in granulomas caused by Mycobacterium tuberculosis. We tested the hypothesis that OPN contributes to host protection in a mouse model of mycobacterial infection. When infected with Mycobacterium bovis BCG, mice lacking a functional OPN gene had more severe infections characterized by heavier bacterial loads and a delayed clearance of the bacteria. The OPN-null mice had greater granuloma burdens consistent with the elevated bacterial load. The ability of osteopontin to facilitate the clearance of mycobacteria was most pronounced early after infection and appeared to be independent of known mediators of resistance to infection by mycobacteria: antigen-specific T-cell immunity, gamma interferon production, and nitric oxide production. BCG grew more rapidly in macrophages derived from OPN-null mice than in those from wild-type mice, demonstrating that the null phenotype was due to an intrinsic macrophage defect. These results indicate that osteopontin augments the host response against a mycobacterial infection and that it acts independently from other antimycobacterial resistance mechanisms.

Animals↗

PubMed1997

Recombinant interleukin-2 in lepromatous leprosy lesions: immunological and microbiological consequences.

Seven patients with lepromatous leprosy (LL) were inoculated with recombinant interleukin-2 (rIL-2) at 5 lesional sites on the back, four sites receiving one dose of 10 micrograms and biopsy specimens being obtained on 4 consecutive days after the injection. At the 5th site, rIL-2 was instead administered over several days, three patients receiving a total dose of 40 micrograms and 4 patients 150 micrograms, while biopsy specimens from this site were obtained 7, 14 and 21 days after the first injection. Most injection sites developed features of a delayed-type hypersensitivity reaction, namely erythema and induration at the injection site, infiltrates rich in T helper cells, monocytes, and Langerhans cells, and at sites receiving higher doses, multinucleated Langhans giant cells and epithelioid granulomas. In some patients, there were favourable shifts in histological classification or small changes in bacterial load. Low doses of rIL-2 injected into LL lesions rapidly enhance cellular immunity and may alter the histological classification or bacterial load at the injection site.

Adolescent↗

PubMedDate not supplied

Dental disease, caries related microflora and salivary IgA of children with severe congenital cardiac disease: an epidemiological and oral microbial survey.

The objectives were to determine levels of dental caries, plaque accumulation, gingival inflammation, knowledge of dental health practices, and oral bacterial loading of S. mutans, Lactobacillus sp., Candida sp., and salivary IgA in the mouths of children afflicted with severe congenital heart disease. A total of 60 children from the cardiac units of the Hospital for Sick Children and Guys Hospital Paediatric Department were compared with 60 case-matched control children from the Department of Orthodontics and Paediatric Dentistry, UMDS (Guys Dental School), London. Using the methodology of the World Health Organization, the decayed, missing and filled surfaces and teeth of primary (dmft) and permanent (DMFT) were compared. There were similar levels of caries in the cardiac (dmft 3.9 and DMFT 2.7) and the control (dmft 3.7 and DMFT 2.0). A significant difference was the proportion of untreated carious lesions in the cardiac group (52%) compared to the control group (32%; P < 0.001). Standard oral microbiological techniques were used to isolate S. mutans, Lactobacillus sp., Candida sp., and conventional methods for estimating salivary IgA. There was no difference between the cardiac and the control group. Children with severe congenital cardiac disease have moderately high levels of dental caries with a significantly greater amount of untreated disease. The high bacterial loading associated with high levels of bacterial dental plaque and gingivitis may put cardiac patients at unnecessary risk of developing bacterial endocarditis.

Adolescent↗

PubMed2004

Analysis of chicken TLR4, CD28, MIF, MD-2, and LITAF genes in a Salmonella enteritidis resource population.

Salmonella enteritidis is a foodborne pathogen that negatively affects both animal and human health. Genetic variations in response to pathogenic SE colonization or to SE vaccination were measured in a chicken resource population. Outbred broiler sires and 3 diverse, highly inbred dam lines produced 508 F1 progeny that were evaluated for either bacterial colonization after pathogenic SE inoculation or circulating antibody level after SE vaccination. Five candidate genes were selected for study, based on their biological function as possibly affecting response to SE: toll-like receptor 4 (TLR4), T-cell specific surface protein (CD28), macrophage migration inhibitory factor (MIF), MD-2, and lipopolysaccharide-induced tumor necrosis factor (TNF)-alpha factor (LITAF). Gene fragments were sequenced from the founder lines of the resource population. The LITAF and MIF genes were homozygous for all sires. Single nucleotide polymorphisms (SNP) were identified in 3 genes (TLR4, CD28, and MD-2) and were used to test for associations of sire SNP with SE response. Linear mixed models were used for statistical analyses. The CD28 broiler sire SNP was associated with both bacterial load in the cecum (P < 0.003) and vaccine antibody response (P < 0.05). The MD-2 SNP was associated (P < 0.04) with the bacterial load in the spleen. The use of these SNP in these genes in marker-assisted selection may result in enhancement of disease resistance.

Animals↗