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At least 19 recordsLinked to original sources
PubMed2026

Proteomic insights into Helicobacter pylori infection in stomach cells, revealing host response and host-targeted therapeutics repurposing.

BACKGROUND: Helicobacter pylori (H. pylori) is a globally prevalent gastric pathogen strongly associated with chronic gastritis, peptic ulcers, and gastric cancer. While bacterial factors have been extensively studied, host proteomic responses and their therapeutic potential remain largely underexplored. RESEARCH DESIGN AND METHODS: Current analyses employed a systematic proteomics-based data integration and harmonization approach (retrospective qualitative cohort study) to identify important differentially regulated host proteins. Proteomic datasets were curated from in vitro studies and analyzed for functional enrichment, protein-protein interaction networks, and hub protein identification. To explore therapeutic repurposing, drug repositioning was performed using the DrugBank database. RESULTS: Data summation describing protein differential regulation in human gastric cells as a result of the infection revealed 1672 perturbed host proteins. Bioinformatics analysis revealed 11 proteins including CSK, MET, RELA, MARK2, GRB2, FTO, PLCG1, CRKL, RPS5, RPS9, and RPS27A to be ideal host targets for therapeutic repurposing. Clinically approved drugs such as Dasatinib (targeting CSK) and Crizotinib (targeting MET) emerged as promising candidates due to favorable pharmacokinetics and known bioactivity. CONCLUSIONS: Host-directed therapeutics could offer alternative strategies to conventional antibiotic therapy, addressing challenges such as resistance and infection recurrence, providing a foundation for future experimental validation and development of host-targeted interventions for infection control.

Humans↗
PubMed1991

Host responses in the etiology and pathogenesis of periodontal disease.

Periodontal disease is an inflammatory condition of the supporting structures of teeth. This condition is actually considered to be caused by a number of different diseases, possibly associated with different etiologies, rather than a single disease. Due to limitations in our present understanding of cellular and molecular events involved in the pathogenesis of various periodontal diseases, many therapeutic failures still occur. For this reason, studies concerning the responses of the host to pathogenic bacteria are thought to be critically important. This review presents current opinions on the role of host responses in periodontal disease.

Antibody Formation↗
PubMed1992

Host responses in periodontal diseases: current concepts.

In periodontal diseases, bacteria trigger inflammatory host responses which, along with the direct destructive effects of the bacteria, cause most of the tissue destruction. Periodontal inflammatory responses are, by and large, immunologic, and our understanding of these reactions has been advanced by the explosion of knowledge in immunobiology, some of which is discussed in this review. Understanding the role of immune cells and their regulatory cell surface molecules such as the MHC, CD antigens, and receptors, as well as knowledge of effector systems set into motion such as phagocytes and cytotoxic T-cells, and the effector molecules such as antibodies, complement, and cytokines, have led to better understanding of the complex pathogenesis of periodontal disease. The role of mediators including the matrix metalloproteinases, proteoglycans, the kinins and anaphylatoxins, and low molecular weight mediators including products of arachidonic metabolism is beginning to be elucidated in periodontal disease. Important avenues of research for development of diagnostic tests based upon host response are apparent. For example, tissue products released during periodontal inflammation including the metalloproteinases, elastase, cytokines, prostaglandins, antibodies, and complement components may provide the basis for future diagnostic indicator tests. The recognition that the neutrophil/antibody/complement axis is critical for protection against periodontal bacteria and that abnormalities in this system often lead to increased periodontal susceptibility provide approaches for the development of diagnostic tests assessing risk. A group of factors which are negative regulators of inflammation including TGF-beta, gamma-interferon, and IL-1 receptor antagonist provide potential for assessment of periodontal disease in remission or in the healing phase. Finally, factors such as HLA associations and the molecular basis for neutrophil abnormalities may provide genetic markers for periodontal disease susceptibility. Diagnostic factors based upon host response measures offer great potential for predicting host susceptibility and will likely be used in combination with microbial diagnostics which identify specific infecting organisms.

Antibody Formation↗
PubMed1977

Host responses to hepatitis B infection in patients in a chronic hemodialysis unit.

Host responses to hepatitis B infection were studied in 222 patients in a chronic hemodialysis unit. From 1970 to 1976, patients were monitored monthly for development of hepatitis B surface antigen (HBsAg), antibody to hepatitis B surface antigen (anti-HBs), and serum transaminase (SGPT) elevations. Five categories of patients were identified as: 1) chronic carriers of HBsAg; 2) transiently HBsAg(+), who developed anti-HBs; 3) HBsAg(-) on admission, who developed anti-HBs without becoming HBsAg(+); 4) anti-HBs(+) on admission; 5) uninfected who remained HBsAg(-) and anti-HBs(-). For a patient who became HBsAg(+) in this clinic, the probability of becoming a chronic carrier was 62-8% and rose to 88.5% if he or she had been HBsAg(+) for five consecutive months. Males were more likely to become chronic carriers, and females were more likely to develop anti-HBs. Neither age, race, nor type of underlying kidney disease was associated with particular host responses to hepatitis B virus. No effect of hepatitis B infection on mortality was detected. Variation in host response to hepatitis B infection among renal dialysis patients may affect the usefulness of hepatitis B hyperimmune globulin and hepatitis B vaccine and be related to the outcome of kidney transplantation.

Antibodies, Viral↗
PubMed1990

The relationship of serum IgG antibody titers to periodontal pathogens to indicators of the host response in crevicular fluid.

In this study; the relationship of indicators of the local host response in gingival crevicular fluid (GCF) to the serum antibody titer to periodontal pathogens was examined. 15 patients with chronic adult periodontitis were studied. GCF was collected and analyzed for the total amount of IgG, IgM, the lysosomal enzyme B-glucuronidase (BG) and alpha-2-macroglobulin (alpha 2M). At the same examination, serum from these patients was collected, and enzyme-linked immunosorbent assays used to determine the serum IgG antibody titer to a panel of 17 periodontal pathogens (Actinobacillus actinomycetemcomitans (3 strains), Bacteroides gingivalis (4), Eikenella corrodens (2), Wolinella recta, Bacteroides intermedius (3), Fusobacterium nucleatum, and 3 Capnocytophaga species). Using Spearman rank order correlation analysis, correlation coefficients were calculated to relate the 4 indicators of host response in GCF to the serum IgG antibody titer to each of the 17 micro-organisms. The mean correlation between total IgG in GCF and the serum IgG antibody titer was positive (r = +0.30), and statistically significant correlations between total IgG in GCF and serum IgG antibody titer were observed for one strain of B. intermedius and C. ochracea. A weaker positive correlation was observed for IgM (r = 0.18). In contrast, the mean correlation between total BG in GCF and the serum antibody titer was negative (r = -0.34). Statistically significant negative correlations were observed for all 3 strains of A. actinomycetemcomitans, one strain of E. corrodens and W. recta. The mean correlation for alpha 2M was r = -0.06. These data suggest that elevated BG activity in GCF, believed to be a marker for lysosomal enzyme released from polymorphonuclear leukocytes in the crevicular environment, may be associated with a reduced serum IgG antibody response to suspected periodontal pathogens. Furthermore, these findings imply that the development of a serum IgG antibody response to suspected periodontal pathogens is consistent with a protective host response.

Actinobacillus↗
PubMed1977

Is multiple sclerosis an age-dependent host response to measles?

A hypothesis is presented that multiple sclerosis (MS) may represent an unusual host response to measles virus, dependent upon when the measles virus is acquired. If acquired late in childhood or near adolescence, the risk of MS is increased. Evidence to support this hypothesis is still meager, but there is ample support from many types of infection for the idea that a host's response may vary with age at the time of infection. As measles virus titers are somewhat increased in MS, evidence for age-dependent alteration in host responsiveness to measles may be taken as further support for the hypothesis. In addition, epidemiologic and clinical data linking MS frequency and average age at the time of measles infection exist. In those areas where MS is rare, measles tends to occur early in life; where MS is common, measles tends to occur later. In case-control studies, measles occurred later in MS patients than in the control groups. Finally mechanisms which might explain an age-dependent alteration in host responsiveness were considered, including maturation of an immune system or maturation of a CNS target cell, e.g. the oligocyte. Additional studies are needed to establish a firmer basis for the concept that risk of MS might be determined, in part, by the age at which a certain infection (e.g. measles) is acquired. If the hypothesis is correct, the mass measles vaccination programs should start to produce a decline in MS frequency. Because the event causing MS is believed to occur before age 15 and MS begins on the average by age 30, a 15-year lag in the effect of measles vaccine on MS frequency is to be expected. Mass measles vaccination was began in 1965, thus by 1980, a decline in MS frequency might be looked for as a test of the hypothesis. Perhaps by the V Pan-American Congress of Neurology, we shall be able to report that MS is disappearing.

Adolescent↗
PubMed1991

Dependence among host response parameters used to diagnose urinary tract infection.

The host-response parameters fever, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) are activated in concert by cytokines such as interleukin-6 (IL-6). Il-6 is secreted in response to Escherichia coli infection of the urinary tract. This study tested the hypothesis that the level of fever, CRP, and ESR is coregulated in individual patients. Body temperature, CRP, ESR, pyuria, and renal concentrating capacity were analyzed in 692 children with first-time urinary tract infections. The association of the parameters was evaluated by correlation and multiple regression analysis. The body temperature, CRP, and ESR were significantly correlated (r = .54, .58, and .58; P less than .001), and variation in CRP and ESR explained approximately 40% of the variation in fever. In contrast, the renal concentrating capacity and pyruia were weakly or not at all correlated with the febrile response (r = -.22; P less than .001), and less than 10% of the variation in renal concentrating capacity was explained by the other parameters. The results suggest that fever, CRP, and ESR describe the same aspect of the host response to UTI.

Adolescent↗
PubMed1976

Is multiple sclerosis an age-dependent host response to measles?

Several lines of evidence support the possibility that multiple sclerosis (M.S.) may be an age-dependent host response to measles. In animals, measles evokes different responses depending upon age at inoculation. In man, measles is already known to produce at least two age-dependent responses: risk of subacute sclerosing panencephalitis is increased among those who have had measles before 2 years of age and risk of measles encephalitis increases with age, at least during adolescence. Studies of immigrant populations indicate that an event at or before adolescence but not infancy affects risk of M.S. In the tropics where M.S. is rare, measles tends to be acquired very early in life, usually before the age of 3, whereas in temperate areas, measles tends to be acquired later, after the age of 5. A retrospective study has shown that M.S. patients tend to have had measles later than controls. Mechanisms which might underlie an age-dependent host response to measles include maturation of an immune system (k.g., number of available B cells) or change in the metabolic state of a target cell (e.g., oligocytes which change from laying down myelin to maintaining it). If the hypothesis that M.S. is a host response to later measles infection is valid, then mass measles vaccination programmes should produce a decline in the rate of M.S., but the effect may not be discernible before 1980.

Adolescent↗
PubMed1976

Host response to tumor-associated fetal antigens: kinetics and components.

Using a colony-inhibition bioassay that measures the contribution of the host response in transplantation immunity to tumor-associated fetal antigens (TAFA), I evaluated the occurrence of TAFA during different developmental stages of murine fetal liver cells. A maximum concentration of TAFA was present at approximately 15 days' gestation. A similar age-equivalence phase of gestation was also found in pig fetal liver. Host-response kinetics to TAFA were examined, and results indicated a similar pattern of activity for tumor- or fetal-immunized groups with a transient immune suppression in the middle of the study period. I detected specific antibodies generated by tumor and fetal cell immunization by a complement-dependent serum microcytotoxicity assay. The specificity of the reaction was evaluated further by absorption studies that demonstrated specific cross-reactive antibodies to fetal and tumor cell targets. Adoptive transplanted immunity to TAFA was indirectly evaluated by a modified Winn assay which indicated that a cellular immune mechanism was an important component of the host response to TAFA.

Animals↗
PubMed1979

Glucocorticoid and antibiotic effects on hepatic microcirculation and associated host responses in lethal gram-negative bacteremia.

Liver changes and associated host responses were evaluated in four groups of male rats, weighing 300 +/- 20 gm., which received intravenous injection of 2.2 times 10(9) live Escherichia coli. This bolus was given either without additional treatment (group A) or prior to the following regimens: intramuscular injection of gentamicin sulfate, 5 mg. per kg. (group B); intravenous injection of methylprednisolone sodium succinate, 40 mg. per kg. (group C); and intramuscular injection of gentamicin immediately after methylprednisolone sodium succinate treatment (group D). Rats given injections of saline or methylprednisolone sodium succinate served as controls. Survival rates at 10 and 20 hours were 25 per cent and 4 per cent for group A; 44 per cent and 28 per cent for group B; 94 per cent and 70 per cent for group C; 98 per cent and 98 per cent for group D, respectively. In rats of groups A and B, killed at 1, 2, 4, and 6 hours, progressive liver changes included intravascular sequestration of rapidly degranulating leukocytes, fibrinous deposits, and platelet aggregates in sinusoids as well as in spaces of Disse adjacent to subendothelial collagen, and extensive Kupffer cell disruption in association with severe midzonal necrosis. These alterations were accompanied by progressive hypoglycemia and elevations of serum enzymes, glutamic pyruvic transaminase, lactate dehydrogenase, and glutamic oxaloacetic transaminase. Hematologic studies revealed that E. coli bacteremia results in rapid leukopenia and disseminated intravascular coagulation primarily due to activation of the intrinsic coagulation pathway. All above reactions were delayed and markedly reduced in rats treated with methylprednisolone sodium succinate. The results indicate that antibiotic treatment of lethal, Gram-negative bacteremia is effective only in conjunction with early steroid treatment. The protective effects of glucocorticoids on the liver microcirculation and polymorphonuclear leukocytes appear to play a basic role in preventing the early development of disseminated intravascular coagulation, hepatocellular necrosis, and associated major host responses, thereby attenuating lethality of gram-negative septic shock.

Animals↗
PubMed1990

Principal lymphocyte subpopulation in local host response to human oesophageal cancer.

We investigated what subpopulations of tumour-infiltrating lymphocytes (TIL) play a key role in in vivo function and what determines the degree of local host response represented by lymphocyte infiltration in human oesophageal cancer. We examined the increased subpopulation of TIL in "good responders" (GR) (patients with intensively TIL infiltrated tumours) when compared with "poor responders" (PR) (patients with weakly TIL infiltrated tumours). The frequency of each subpopulation was determined by quantitative flow-cytometric measurement on TIL separated from fresh tumours. Of TIL in GR, the frequency of CD3+ cells increased significantly (P less than 0.05) but the frequencies of CD16+, Leu7-, and CD16+ Leu7- cells were low and did not increase significantly compared with those in PR. With respect to T-cell subsets of TIL in GR, the frequency of CD8+ cells was significantly higher than that in PR (P less than 0.01), and CD4+/CD8+ ratio was lower than that in PR (P less than 0.025). On two-colour analyses, most of CD8+ cells (cytotoxic/suppressor T-cells: Tc/s) did not co-express CD11b and the frequency of CD8+ CD11b- cells (cytotoxic T-cell: Tc) increased significantly compared with that in PR. Clinicopathological and phenotypic analysis of peripheral blood lymphocytes revealed that there are no major differences in general immunocompetence between GR and PR. These results suggest that Tc/s, especially Tc, might play a key role in local host response. They also suggest that not only the general immune status of the host but also the identification of class I major histocompatibility complex antigens by the host at the tumour site may strongly affect the degree of host response in oesophageal cancer.

Aged↗
PubMed1991

Lyme borreliosis: host responses to Borrelia burgdorferi.

The chronic inflammatory condition that develops after infection by B. burgdorferi is a complex process resulting from host responses to a limited number of organisms. Amplification mechanisms driven by potent proinflammatory molecules, i.e., IL-1, may explain the vigorous response to a paucity of organisms. Spirochete dissemination to distant locations involves adherence to and penetration across endothelium and may be facilitated by host responses that increase vessel permeability. The apparent lack of tissue tropism in Lyme disease is reflected in the organism's ability to adhere to different eucaryotic cell types in vitro and the wide distribution of B. burgdorferi in various organs of infected humans and experimentally infected animals. While phagocytosis and complement activation have been observed in vitro, the specific immune response that develops in humans is inefficient in eradicating the organisms, which may possess some mechanism(s) to evade this response. There is significant evidence for host autoreactivity based on antigenic cross-reactivity between the 41-kDa flagellar subunit and stress proteins of the spirochetes and endogenous host cell components. Although the outer surface proteins appear to be suitable candidates as targets for vaccination in animal studies, fundamental differences in the immune response to spirochetal components may preclude their use in humans.

Animals↗
PubMed1975

Host response to infection by Coxiella burneti.

A host response to infection by Coxiella burneti was investigated. Infectedyolk sacs were harvested from embryonated eggs and assayed for glycolytic activity. Assays of glycolytic enzymes included glucose isomerase, aldolase, phosphofructokinase,fructose-1,6-diphoshatase, glyceraldehyde-3-phosphate dehydrogenase, enolase, and pyruvate kinase. No significant differences in enzymatic activity between normal and infected tissues through the 12th day was observed. From the 13th day through the 16thday, the glycolytic activity of normal tissues decreased. Glycolytic activity of infected tissues did not decrease, but showed a gradual increase during this same time period. Embryos from infected eggs demonstrated a gradual decrease in total weight fromthe 12th day until death occurred on the 16th day.

Animals↗
PubMed1991

Host responses and neuroendocrinological changes in pyrexia in childhood.

Host responses and neuroendocrinological changes during pyrexia in childhood were studied. Serum IL-1 beta could not be detected in most subjects either during pyrexia or in afebrile periods. IL-1 beta was detected in two cases, increasing during pyrexia and decreasing during the afebrile period. Plasma ACTH increased during pyrexia, but this was not statistically significant. Serum cortisol during pyrexia increased to around twice the normal value, and many subjects showed a high level of arginine vasopressin. The subjects, who did not develop dehydration, showed a decrease in serum osmolality and serum sodium during the pyrexia period. Serum Fe and Zn decreased, but serum Cu increased during both periods. It could not be confirmed that IL-1 activates the hypothalamic-pituitary-adrenal axis during pyrexia. It is concluded that AVP is important in the control of fever and the maintenance of homeostasis of body fluid during pyrexia.

Acute Disease↗
PubMedDate not supplied

Local cellular host response induced by Nocardia-delipidated cell mitogen in Lewis lung carcinoma-bearing mice.

Various Nocardial fractions have been shown to exert inhibitory effects against several experimental tumors, via a host response mechanism. With the aim of obtaining further information on the mechanism of action of these immunomodulators, we examined in the present study the local cellular host response induced by intratumoral administration of one of these fractions, the Nocardia-delipidated cell mitogen (NDCM), at the site of the tumor (Lewis lung carcinoma-3LL). The tumor itself was found to provoke a scanty cellular infiltration surrounding the tumor mass, mainly composed of lymphocytes. The site of the tumor in NDCM-treated mice was surrounded by a very thick rim of inflammatory cells, consisting of macrophages and lymphocytes. Although recognized decades ago, the existence of tumor infiltrating leukocytes still constitutes a puzzle. The composition and significance of these host cells, in both non-treated and treated tumors has not yet been elucidated. Since lymphocytes were also found around non-treated tumors and they apparently did not prevent tumor development, it is possible that macrophages play a more important role in the NDCM-elicited host defense against the Lewis lung carcinoma.

Animals↗
PubMed1990

Host responses in mediating sepsis and adult respiratory distress syndrome.

Despite significant advances in intensive care unit technology and mechanical ventilatory support, mortality due to adult respiratory distress syndrome (ARDS) or multiorgan failure (MOF) has not changed significantly within the past two decades. The key to improving survival requires understanding and modifying (or eliminating) factors that may initiate (or modulate) these syndromes. Infection, and the host responses to infection, are major etiological factors responsible for the induction and perpetuation of the injury to the lung and microvasculature in ARDS and MOF, and contribute to late mortality. While the pathogenesis of ARDS and MOF-complicating sepsis remains to be elucidated, bacterially derived (eg, endotoxin or lipopolysaccharides [LPS]) and host-derived humoral and cellular mediators are of importance in both disease states. In fact, the host response to infection (or injurious stimuli) may be a more critical determinant of the outcome of sepsis and ARDS than the original inciting stimulus. The pleiotropic effects of LPS are largely indirect, and are orchestrated via its ability to trigger the release of an array of host-derived mediators of inflammation. Several potential mechanisms of injury in ARDS, sepsis, and MOF have been suggested and include a variety of inflammatory cells (neutrophils, mononuclear phagocytes, platelets), activated complement and coagulation components, vasoactive mediators (kinins, arachidonic acid metabolites, lipids, peptides), reactive oxygen radicals, and diverse cytokines. Interactions between these humoral and cellular mediators appear to set in motion an amplified cascade of events culminating in cellular and tissue injury. In this article, several of these putative inflammatory mediators are discussed in detail, and the importance of cytokine networking and the possible role of nonimmune cells in the orchestration of the inflammatory response associated with ARDS and MOF are explained. Finally, future therapeutic strategies aimed at blocking or suppressing the release or effects of endogenous mediators may be the key to improving the outcome of these disorders.

Arachidonic Acid↗
PubMed1990

A comparison of host responses of the Mongolian jird to infections of Brugia malayi and B. pahangi.

Host responses of jirds receiving a single subcutaneous inoculation of subperiodic Brugia malayi were compared with those of jirds similarly infected with B. pahangi. Parasite burdens, lymphatic lesion severity, granulomatous reactivity, antibody responses to parasite antigens, and complete blood cell counts were assessed at 60 and 150 days post-inoculation. At 60 days post-inoculation, percentages of adults recovered at necropsy and lymphatic lesion severity were greater in B. pahangi-infected jirds. At 150 days post-inoculation, lesion severity and percentages of worms recovered were similar in both infections. No significant differences were noted in either infection in reactivity to homologous or heterologous parasite antigens in any parameter measured. Similarities in the kinetics of the inflammatory reactivities of the 2 infections suggest that previous observations made in the jird-B. pahangi model could be utilized in designing studies using B. malayi. Further, the more marked lesion severity observed in B. pahangi-infected jirds and the relative ease of maintaining B. pahangi in the laboratory support the continued use of this system as a conceptual model for the study of lymphatic lesion pathogenesis.

Animals↗