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Results for “host immune response”

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At least 19 recordsLinked to original sources
PubMed2023

Strain-specific alterations in gut microbiome and host immune responses elicited by tolerogenic Bifidobacterium pseudolongum.

The beneficial effects attributed to Bifidobacterium are largely attributed to their immunomodulatory capabilities, which are likely to be species- and even strain-specific. However, their strain-specificity in direct and indirect immune modulation remain largely uncharacterized. We have shown that B. pseudolongum UMB-MBP-01, a murine isolate strain, is capable of suppressing inflammation and reducing fibrosis in vivo. To ascertain the mechanism driving this activity and to determine if it is specific to UMB-MBP-01, we compared it to a porcine tropic strain B. pseudolongum ATCC25526 using a combination of cell culture and in vivo experimentation and comparative genomics approaches. Despite many shared features, we demonstrate that these two strains possess distinct genetic repertoires in carbohydrate assimilation, differential activation signatures and cytokine responses signatures in innate immune cells, and differential effects on lymph node morphology with unique local and systemic leukocyte distribution. Importantly, the administration of each B. pseudolongum strain resulted in major divergence in the structure, composition, and function of gut microbiota. This was accompanied by markedly different changes in intestinal transcriptional activities, suggesting strain-specific modulation of the endogenous gut microbiota as a key to immune modulatory host responses. Our study demonstrated a single probiotic strain can influence local, regional, and systemic immunity through both innate and adaptive pathways in a strain-specific manner. It highlights the importance to investigate both the endogenous gut microbiome and the intestinal responses in response to probiotic supplementation, which underpins the mechanisms through which the probiotic strains drive the strain-specific effect to impact health outcomes.

Mice↗
PubMed2024

RNA editing in host lncRNAs as potential modulator in SARS-CoV-2 variants-host immune response dynamics.

Both host and viral RNA editing plays a crucial role in host's response to infection, yet our understanding of host RNA editing remains limited. In this study of in-house generated RNA sequencing (RNA-seq) data of 211 hospitalized COVID-19 patients with PreVOC, Delta, and Omicron variants, we observed a significant differential editing frequency and patterns in long non-coding RNAs (lncRNAs), with Delta group displaying lower RNA editing compared to PreVOC/Omicron patients. Notably, multiple transcripts of UGDH-AS1 and NEAT1 exhibited high editing frequencies. Expression of ADAR1/APOBEC3A/APOBEC3G and differential abundance of repeats were possible modulators of differential editing across patient groups. We observed a shift in crucial infection-related pathways wherein the pathways were downregulated in Delta compared to PreVOC and Omicron. Our genomics-based evidence suggests that lncRNA editing influences stability, miRNA binding, and expression of both lncRNA and target genes. Overall, the study highlights the role of lncRNAs and how editing within host lncRNAs modulates the disease severity.

Biological sciences↗
PubMed1978

The role of the host immune response in the development of tissue lesions associated with African trypanosomiasis in mice.

A variety of tissue lesions occurs in African trypanosomiasis, in the pathogenesis of which direct toxic effects of the parasite as well as immunological mechanisms may be involved. The purpose of the present study was to evaluate the role of the host immune response in inducing tissue damage in this disease and particularly in the production of lesions in striated muscle. The development of muscle lesions in T. brucei infection was studied in several groups of mice with different forms of immunodeficiency, as well as in normal mice. In the normal mice, foci of intense inflammation and necrosis were found in the cardiac and skeletal muscles 2 weeks or more after infection. In these lesions, there was a heavy deposition of IgG and IgM, and of trypanosomal antigens. In irradiated, newborn mice, and athymic nude mice infected with T. brucei, these inflammatory lesions were not found, although large numbers of trypanosomes were present between the muscle fibres. The characteristic lesions could be induced in athymic nude mice by transfer of normal spleen cells or of normal T lymphocytes 1 week after the onset of infection. The lesions were also partly induced by transfer of antibody to T. brucei. No antibodies to tissue components, particularly to cardiac myofibrils, were found in any of the infected mice. The results of this study show that immunodeficiency suppresses the development of the characteristic muscle lesions of African trypanosomiasis. The relative importance of humoral and cellular immune mechanisms in the pathogenesis of these lesions is not year clear.

Animals↗
PubMed1979

The possible role of the frontal and sub-parietal gland systems of the pentastomid Reighardia sternae (Diesing, 1864) in the evasion of the host immune response.

The frontal and sub-parietal glands of the pentastomid Reighardia sternae elaborate lamellate secretion which is poured on to the cuticle. The entire surface of the cuticle, including the mouth, hook pits and reproductive apertures, is coated with secretion. Electron microscope studies indicate that the glands are continuously active, which implies a turnover of surface membranes. The postulated function of these membranes is to protect certain vital areas of the host--parasite interface, notably the pores of ion-transporting cells, from the host immune response. The available evidence suggests that pentastomids do evoke a strong immune response but since most are long-lived they must circumvent it. We believe the surface membrane system to be instrumental in this. Studies on another pentastomid, Porocephalus crotali in rats have shown that an immune response stimulated by a primary infection will kill subsequent infections and that the surface membranes are strongly immunogenic. Obvious parallels between this situation and that of schistosome infections in mammals are discussed. An alternative explantation of concomitant immunity is proposed.

Animals↗
PubMed1976

Cytomegalovirus replication and the host immune response.

Cytomegalovirus (CMV) is closely associated with host cellular structures, and this has a significant impact upon the immunologic response following infection. CMV may be recovered from a variety of body secretions and fluids during acute infection, and protracted shedding may supervene in some instances. The reasons for a variable host response to CMV infection remain unclear, and the mechanisms responsible for the establishment of persistence have not been worked out. CMV persistence and latency are discussed, and some recently derived relevant data are presented. An animal model has been developed consistent with clinical observations pertaining to CMV transmission with blood. Results obtained in the course of these and other studies support the concept of immunological activation of latent CMV. The timing of CMV infection relative to an unrelated antigenic challenge is probably critical in determining the emergence of immunodepression or enhancement. Some aspects of CMV sero-diagnosis are also reviewed.

Animals↗
PubMed2025

Helminth infections affect host immune responses to viral infections and vaccines.

Helminths are highly prevalent in many regions of the world. Due to the chronic nature of most helminth infections, these parasites are proficient immunomodulators of their hosts. This modulation often leads to skewed or even impaired immune responses against unrelated antigens, such as viruses and vaccines, which can be both beneficial and detrimental for the host. The extent of these effects and the impact on the outcomes of viral infection depends on a variety of factors including timing and tropism of both infections, pathological mechanisms, genetic background, and environmental factors. In this review, we dissect these complex interactions between virus and helminths in the context of coinfection and the impact of helminth infection on antiviral vaccine efficacy. We characterize the key contributing mechanisms that have been defined in preclinical models and human trials and describe the immune actors involved in the modulation of the antiviral and vaccine immune response by helminths. Finally, we address the limitations of our current understanding of helminth-virus interactions.

Helminthiasis↗
PubMed1976

Immune host response to corneal grafts sensitized to herpes simplex virus.

Experiments were performed to study the fate of corneal grafts sensitized to herpes antigens when grafted to HSV-sensitized hosts. Nonsensitized grafts in systemically sensitized hosts remained clear, whereas all locally sensitized grafts in systemically sensitized hosts became opaque within ten days. The stroma showed severe lymphocytic and plasma cell infiltration and neovascularization. One-half of the corneas from systemically sensitized hosts grafted to eyes previously infected opacified in an accelerated manner. Round cells were found in the stroma and endothelium. The histological reaction in both groups was similar to that found in the immune graft reaction even though the clinical picture was not typical (peripheral and progressive edema with a rejection line). The accelerated reaction was probably related to the presence of virus antigens in graft stroma and subepithelial areas of the graft. The significance of HSV-sensitized donor tissue grafted onto HSV-sensitized hosts is discussed because of its possible implication in tissue transplantation.

Animals↗
PubMed1979

Host immune responses after administration of inactivated Venezuelan equine encephalomyelitis virus vaccines--III. Kinetics for neutralizing antibody immunoglobulin class responses in donors and adoptively-immunized recipients.

C57B16 mice were immunized with either live, attenuated TC-83 strain VEE virus vaccine or formalin-inactivated VEE vaccine combined with Bordetella pertussis. The kinetics of specific donor and adoptively-immunized recipient anti-VEE neutralizing antibody responses were studied. Donor mice immunized with either live or inactivated VEE virus vaccine combined with potent adjuvants develop specific anti-VEE IgM and IgG responses as early as 7 days post-immunization. Anti-VEE IgM antibody responses comprise the majority of anti-VEE neutralizing antibody at this early time period. By 14 to 21 days post-immunization, anti-VEE IgG responses predominated. When adoptively-immunized recipients were studied, the anti-VEE IgM to IgG predominance seen in donors early after administration was reversed, and for each time-period studied, recipients' serum anti-VEE antibody class responses consisted principally of IgG rather than IgM antibody. Since T-cells cooperation with B-cells is critical in the IgM-IgG antibody shift, these studies support the critical role T-cells exert in adoptive transfer in a murine model of experimental VEE infection. Furthermore, immunization with either live or inactivated VEE vaccine coupled to a potent adjuvant induce comparable donor and adoptively-immunized recipient anti-VEE antibody class responses.

Animals↗
PubMed1979

The tumor dormant state. Quantitation of L5178Y cells and host immune responses during the establishment and course of dormancy in syngeneic DBA/2 mice.

Subcutaneous implantation of DBA/2-derived L5178Y cells into DBA/2 mice followed 10 d later by nodule excision protected 100% of mice from the rapid outgrowth of an intraperitoneal challenge of L5178Y cells given 7 d postexcision. Challenged mice remained clinically normal for 48--250 d before onset of an ultimately fatal tumor outgrowth. The numbers of L5178Y cells in the peritoneal cavity increased logarithmically for 4 d after challenge and then declined to low but detectable levels which persisted throughout the clinically normal period. Cells active in 18-h in vitro cytolytic assays against 51Cr-labeled L5178Y target cells were found in the peritoneal cavity. The effector cells were determined to be Thy1.2 positive. Their activity was tumor specific and reached peak levels 4 d after tumor challenge and then gradually declined to undectable levels during the following 70 d. Tumor emergence occurred most frequently during the period when CMC activity was no longer demonstrable in the remaining clinically normal mice. A transient peak of low level cytophilic antitumor antibody was detected about 30 d after tumor cell challenge. The temporal associations between the numbers of tumor cells and the levels of cell-mediated lysis against L5178Y cells indicate the importance of the cell-mediated cytolysis response in limiting initial tumor outgrowth and suggest its role as one of the factors responsible for long-term tumor suppression during tumor dormancy.

Animals↗
PubMed1976

Host immune responses after administration of inactivated Venezuelan equine encephalomyelitis virus vaccines. I. Description and characterization of adoptive transfer by immune spleen cells.

Cellular immune responses after immunization with a number of inactivated Venezuelan equine encephalomyelitis (VEE) virus vaccines were evaluated in mice by means of an adoptive transfer system. Formalin-inactivated, TC-83 strain VEE virus vaccine was immunogenic and highly effective in protecting recipient mice against challenge with virulent VEE virus. In contrast to immunization with live TC-83 VEE virus vaccine, however, immunization with inactivated VEE vaccine did not provide donor mice with the capacity to transfer adoptive immunity readily. Only when mice were immunized with inactivated VEE vaccine combined with specific adjuvants (particularly complete Freund's adjuvant or Bordetella pertussis) were donors capable of consistently transferring adoptive immunity. The total dose of inactivated VEE vaccine did not appear to influence the capacity to transfer adoptive immunity. On the other hand, weekly boosters of VEE vaccine and/or administration of vaccine with specific adjuvants did markedly influence donor immune responses.

Animals↗
PubMed1976

Host immune responses after administration of inactivated Venezuelan equine encephalomyelitis virus vaccines. II. Kinetics of neutralizing antibody responses in donors and adoptively immunized recipients.

Lymphoid cell responses to immunization with various formalin-inactivated Venezuelan equine encephalomyelitis (VEE) virus vaccines were monitored in mice by assessment of the development of both the neutralizing antibody response in sera of spleen cell donors and the adoptive neutralizing antibody response induced by spleen cell transfer in recipients. Donors immunized intraperitoneally with formalin-inactivated VEE vaccine (a single dose or a dose on three consecutive days) developed early serum neutralizing antibody responses (larger than or equal to 1:88-1:100) by seven days after immunization. Recipients of spleen cells from such mice were, however, incapable of eliciting a neutralizing antibody response (less than or equal to 1:10). Only spleen cells from donors immunized with inactivated VEE vaccine plus adjuvants (particularly complete Freund's adjuvant and Bordetella pertussis) were consistently capable of producing early, high-titer serum neutralizing antibody responses in adoptively immunized recipients (larger than or equal to 1:50-1:120 on day 4). The magnitude of neutralizing antibody responses of donors to inactivated VEE vaccines did not serve as a useful indicator of whether spleen cells from such mice could adoptively induce antibody responses in recipients. Finally, treatment of immune spleen cells with rabbit antiserum to mouse thymocytes, but not with rabbit antiserum to mouse gamma-globulin or normal rabbit serum, abolished the capacity of such cells to transfer an antibody response adoptively.

Adjuvants, Immunologic↗
PubMed1977

Role of host immune response in the development of either encephalitic or paralytic disease after experimental rabies infection in mice.

The clinical and histopathological manifestations of the infection of immunosuppressed (cyclophosphamide-treated) and immunocompetent (control) adult mice with the CVS ts 2 strain of fixed rabies virus were correlated with the kinetics of virus multiplication in the central nervous system and with the development of serum antibody. In immunocompetent mice severe paralytic disease causing 80% mortality was accompanied by marked inflammation and degeneration of the central nervous system parenchymatous tissue. Antirabies antibody was detected in all immunocompetent mice severely paralyzed from postinoculation day 6 on; virus was rarely isolated. In contrast, immunosuppressed mice developed encephalitic symptoms with only minor paralysis; the infection was 100% fatal. Histopathological changes in immunosuppressed mice were confined to degeneration and necrosis of individual neurons and mild microglial reaction; virus was isolated from all of these mice. No significant level of antibody was detected. Similar manifestations were seen after infection of immunodeficient (athymic) mice except that the athymic mice developed levels of antibody similar to those of control mice on day 6; antibodies in athymic mice were predominantly of immunoglobulin class M.

Animals↗
PubMed1976

[Infection due to hepatitis B virus and host immune response].

Cell-mediated immunity (CMI) to hepatitis B surface antigen (HBsAg) was investigated in patients who recovered from acute hepatitis B and in chronic carriers of the antigen, either with or without liver disease. The study was performed using leucocyte migration inhibition test and purified HBsAg. In antigen-negative post-hepatitis patients the frequency of cellular immunity to HBsAg (63.6%) showed a significant difference to controls. On the other hand, only one out of 5 antigen-positive post-hepatitis patients showed sensitisation to HBsAg; four out of these cases had chronic hepatitis at liver biopsy. In HBsAg-chronic carriers, with or without liver disease, the frequency of CMI to HBsAg was not significant to controls. A significant correlation was noted between inflammatory activity and inhibition of migration. Our results suggest that a normal cellular immune response to HBsAg is necessary for the recovery from acute hepatitis B and for the clearance of the virus. In HBsAg-chronic carriers this response seems to be absent or inadequate, leading to the state of healthy chronic carriers or to the evolution to HBsAg-chronic hepatitis, respectively. The high frequency of CMI in HBsAg-negative chronic active hepatitis, suggests that hepatitis B virus infection may play a role in the ethiology of the disease.

Antibodies, Viral↗