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PubMedDate not supplied

Differential effect of aging on membrane immunoglobulin (mIg)-mediated endocytosis in the inductive and effector sites of the mucosal immune system.

The effect of aging on the endocytosis of anti-immunoglobulin (Ig) antibody as ligand by membrane Ig receptors (mIg) of B cells in the spleen, the mesenteric lymph nodes (MLN), and the Peyer's patches (PP) was investigated. Horse radish peroxidase (HRP) labelled (Fab')2 anti-mouse Ig specific for IgM, IgG, and IgA was used as the ligand. The rate of mIg mediated ligand endocytosis by aged B cells was significantly reduced in the PP as compared to the young group. In contrast, there were no age-related differences in the rate of mIg-mediated ligand endocytosis by B cells in the spleen and MLN. After 2 hr of incubation, about 70-80% of ligand added was internalized by splenic and MLN B cells from both young and old mice. Aged PP B cells showed significantly slower rate of ligand internalization as compared to those cells from young mice. This effect was pronounced at 30 and 60 min after incubation. Young PP B cells were found to internalize about 50% of the ligand within 30 min, while it took 60 min for aged B cells to internalize the same amount. The age-related rate of mIg-mediated endocytosis by B cells in the MLN, as opposed to a slower rate of endocytosis by B cells in the PP, emphasizes its distinct nature as a mucosal site.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed2006

Gut ischemia-reperfusion affects gut mucosal immunity: a possible mechanism for infectious complications after severe surgical insults.

OBJECTIVE: To examine influences of gut ischemia/reperfusion (I/R) on gut-associated lymphoid tissue (GALT) mass and function. DESIGN: Prospective, randomized controlled study. SETTING: Research laboratory. SUBJECTS: Male Institute of Cancer Research mice. INTERVENTIONS: Ninety mice were randomized to three groups: I/R (60-min gut ischemia), sham (laparotomy only), and control (no operation). On days 1, 2, 4, 7, and 10, mice were killed to harvest lymphocytes from Peyer patches, the intraepithelial space, and the lamina propria (LP) of the small intestine. Respiratory tract and small intestinal washings were also obtained. MEASUREMENTS AND MAIN RESULTS: Gut I/R significantly reduced lymphocyte numbers in Peyer patches, the intraepithelial space, and the LP. The reduction was prominent in GALT effector sites, that is, the intraepithelial space and LP, but numbers recovered quickly in LP. Changes in cell numbers in Peyer patches, GALT inductive sites, were subtle but persistent. Gut I/R reduced B cell numbers in Peyer patches; alphabeta T cell receptor (TCR)+, gammadeltaTCR+, CD8+, and B cell numbers in the intraepithelial space; and gammadeltaTCR+, CD8+, and B cell numbers in the LP, in comparison with the sham or control group. There were no significant differences in respiratory tract immunoglobulin A levels between the I/R and sham groups. Intestinal immunoglobulin A was elevated on day 1 in the I/R group, with no significant difference after day 2 in comparison with the sham group. CONCLUSIONS: Despite the maintained mucosal immunoglobulin A level, gut I/R markedly reduces GALT cell numbers, with changes in lymphocyte phenotypes. These alterations may be associated with increased morbidity due to infectious complications after severe surgical insults.

Animals↗
PubMed1992

An in vivo study of a glycoprotein gIII-negative bovine herpesvirus 1 (BHV-1) mutant expressing beta-galactosidase: evaluation of the role of gIII in virus infectivity and its use as a vector for mucosal immunization.

We constructed a recombinant BHV-1 in which the glycoprotein gIII gene was replaced by the Escherichia coli lacZ gene. The resultant virus mimics the simple gIII deletion mutant in its growth characteristics in cell culture; however, it expresses beta-galactosidase in virus-infected cells. Further characterization of its virulence and the immune responses elicited by it was conducted in cattle. The mutant virus retained the ability to establish an infection when administered intranasally. Infected animals were also capable of transmitting virus to sentinel penmates. However, the mutant virus showed a reduced replication efficiency in the respiratory tract of cattle, as manifested by significantly lower virus shedding and a shorter duration of shedding when compared to wild-type (wt) BHV-1 infections. The mutant virus induced an efficient anti-BHV-1 antibody response and convalescent cattle were fully protected from subsequent wt virus challenge. In addition, cattle infected with the lacZ-expressing virus developed antibodies to beta-galactosidase. Our results demonstrate that the presence of gIII is not a prerequisite for BHV-1 infection; however, gIII does play an important role in maintaining virus replication efficacy in its natural host. With respect to developing BHV-1 as a vaccine vector, our results indicate that deletion of the gIII gene, which partially attenuates the virus and serves as a vaccine virus marker, does not compromise immunogenicity to BHV-1. Most importantly, this vector is effective in delivering foreign antigens to mucosal surfaces of the respiratory tract.

Animals↗
PubMed1997

A temporal study of TPN-induced changes in gut-associated lymphoid tissue and mucosal immunity.

BACKGROUND: Total parenteral nutrition (TPN) is associated with decreases in small-intestinal gut-associated lymphoid tissue (GALT) T cells, B cells, and IgA levels and impairs IgA-mediated defenses in the respiratory tract. The impaired respiratory tract defenses are speculated to be due to reduced respiratory tract IgA levels. OBJECTIVES: To determine the time course of GALT cell reductions and document any changes in respiratory tract IgA levels in mice receiving TPN. DESIGN: Prospective randomized trial. SETTING: Animal research laboratory. MATERIALS: Thirty-five male ICR mice weighing 25 to 35 g. INTERVENTIONS: Mice underwent cannulation with intravenous catheters and received chow for 2 days followed by TPN for 0 (n=6), 1 (n=6), 2 (n=6), 3 (n=6), 4 (n=6), or 5 (n=5) days. Mice were killed after receiving TPN their respective number of days. The small intestine was harvested, and washings were obtained from the small intestine and the respiratory tract. Lymphocytes and IgA levels were analyzed by flow cytometry and enzyme-linked immunosorbent assay, respectively. MAIN OUTCOME MEASURES: Lymphocyte yields from Peyer patches, intraepithelial spaces, and the lamina propria; IgA levels from the small intestine and the respiratory tract. RESULTS: T- and B-cell yields in the Peyer patches and lamina propria were significantly reduced by day 2 (P<.05) and thereafter compared with day 0. The lamina propria CD4+/CD8+ ratio declined significantly by day 4 (P<.05) compared with day 0. Small-intestinal and respiratory tract IgA levels were significantly diminished by day 3 (P<.05) and thereafter compared with day 0. CONCLUSION: Total parenteral nutrition produces rapid changes in GALT cell profiles and reduces respiratory tract IgA levels consistent with the impairment of respiratory IgA-mediated defenses.

Animals↗
PubMed1993

Age influences recovery of systemic and mucosal immune responses following acute depletion of CD4 T cells.

We have examined the influence of recipient age on the recovery of the CD4 T cell compartment following in vivo treatment with anti-CD4. Mice were treated with anti-CD4 beginning in utero (adolescent), at 8 weeks (young adult), or at 52 weeks (old adult). Following acute CD4 depletion, adolescent mice recovered CD4 T cells rapidly (99% of age-matched controls at 5 weeks after anti-CD4 treatment). Young adult mice recovered more slowly (48% of control at 5 weeks), while old adult mice recovered less than 50% of control CD4 T cell numbers at 12 weeks after depletion. At 12 weeks after anti-CD4 treatment, adolescent mice made an enhanced anti-SRBC antibody response and young adult mice mounted a response comparable to their age-matched controls. In comparison, old adult mice mounted on anti-SRBC response that was only 57% that of their age-matched controls. By 1 week after cessation of anti-CD4 treatment, adolescent mice mounted normal systemic and intestinal responses to challenge with the thymic-dependent antigen cholera toxin (CT). In contrast, young adult mice recovered < 50% of age-matched control CT responsiveness by 5 weeks post-CD4 depletion. By 5 weeks post-CD4 depletion, young adult mice exhibited normal tolerance following enteric tolerization with ovalbumin. These findings underscore the importance of recipient age in designing or interpreting studies employing T cell depletion.

Aging↗
PubMed1998

The spleen and organized lymph nodes are not essential for the development of gut-induced mucosal immune responses in lymphotoxin-alpha deficient mice.

Lymphotoxin knock-out (KO) mice generate specific immune responses to orally administered immunogens despite having neither gut-associated nor peripheral lymphoid tissues. The spleen, therefore, was expected to play a role in the generation of immune responses in these KO mice. KO and wild-type (wt) mice were splenectomized and orally immunized with Salmonella typhimurium. Splenectomy produced the most profound effects on serum and fecal IgA levels in KO mice. Total and antigen-specific serum and fecal IgA were increased in splenectomized wt mice but decreased in splenectomized KO mice. Antigen-specific serum IgG was decreased in both KO and wt splenectomized mice while total IgG increased in splenectomized wt mice. Both splenectomized wt and KO mice demonstrated a compensatory expansion of the lamina propria compartment characterized by a significant increase in the number of IgA spot-forming cells. KO mice demonstrated further compensation for the loss of the spleen in the accelerated development of ectopic lymphoid tissues. We conclude that the spleen plays a prominent role as a lymphoid organ in KO mice but its removal does not abolish immune responsiveness. Residual immune responsiveness in splenectomized KO mice following oral immunization appears to be due to expansion and/or development of alternate effector compartments.

Animals↗
PubMed2000

Orally administered lead chloride induces bias of mucosal immunity.

The hypothesis that lead disturbs gut immune functions upon oral ingestion was tested. Long-term exposure to oral PbCl(2)for 10 days caused persistent downregulation of TGF-beta mRNA levels in intestinal tissue. PbCl(2) also disturbed oral tolerance induction to the dietary antigen ovalbumin. Upon challenge with an immunizing dose of ovalbumin and rechallenge of draining lymph node cells in vitro, tolerance induction was partially suppressed in animals exposed to oral PbCl(2). This was shown by increased proliferation to antigenic stimulus, increased production of IFN-gamma and decreased secretion of TGF-beta. In conclusion, we show for the first time that oral exposure to PbCl(2)has a significant effect on the gut immune system, demonstrated by a bias of the cytokine pattern towards Th(1)and by disturbed oral tolerance mechanisms.

Administration, Oral↗
PubMed2001

Induction of intestinal rotavirus-specific antibodies in respiratory, but not gut, lymphoid tissues following mucosal immunization of mice with inactivated rotavirus.

Intranasal (i.n.), but not oral, immunization of mice with inactivated rotavirus induces protection against challenge. To understand the mechanisms by which i.n. immunization with inactivated rotavirus evokes protective immunity, we examined the site of rotavirus-specific B cell activation and the origins of intestinal IgA-secreting B cells following i.n. inoculation of mice with inactivated rhesus rotavirus. We found that (1) i.n., but not oral, inoculation induced partial protection after challenge; (2) i.n., but not oral, inoculation induced production of rotavirus-specific IgM, IgA, and IgG by intestinal lymphoid tissues; and (3) after i.n. inoculation, nasal-associated lymphoid tissues (NALT) and bronchial lymph nodes (BLN) were the sites of initial production of rotavirus-specific antibodies. These studies indicate that after inoculation with inactivated rotavirus, virus-specific effector B cells may be more easily activated in respiratory, compared to intestinal, lymphoid tissues. Additional studies are needed to determine if these observations are due to fundamental differences in the microenvironment of NALT and BLN compared to Peyer's patches or are a function of the anatomic differences between the respiratory and the gastrointestinal tracts.

Administration, Intranasal↗