Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30)


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Introduction

Multifunctional T cells are the potential correlates of protection against HIV. Most cytokine-expressing cells were positive for only a single cytokine Figures 6 a and 6 b. There was a drop in single-positive cells concurrent with decreased frequencies of multifunctional cells, suggesting that the function of T cells is destroyed. These data suggest that, in addition to activating T cells, LPS influences their functional phenotypes.

These findings suggest that changes in T cell function during LPS stimulation become important factors for immune activation and viral replication inhibition. To identify hematological changes that are associated with LPS treatment, we examined longitudinal hematology data during LPS treatment. Most hematological parameters remained unchanged during LPS treatment data not show , while the number of leukocytes, monocytes, and neutrophils increased rapidly at day 1 in response to LPS treatment Figures 7 a , 7 b , and 7 c. Levels of leukocytes a were increased in LPS-treated Ch-RMs with concomitant increases in monocytes b and neutrophils c.

Platelet counts d were decreased after LPS stimulation. The percentages of monocytes e and neutrophils f were increased in blood. The leukocytes are the first line of immune defense against infection and respond rapidly to LPS. Elevated levels of leukocytes can be the result of inflammatory response and immune activation. A temporary drop in the circulating platelet counts were observed at day 1 after LPS treatment. We speculate that the decrease of platelet counts may be caused by increased activation and subsequent sequestration of platelets in platelet-monocyte aggregates as reported by Metcalf Pate et al.

Persistent immune activation is a hallmark of progressive HIV infection. The level of immune activation is more closely associated with disease progression compared to plasma VL [ 31 ]. Plasma levels of LPS are closely associated with the intestinal permeability degree. Accumulative evidence indicates that microbial translocation MT promotes systemic immune activation in chronic HIV infection [ 1 ]. As previously reported, the translocation of LPS contributes to the systemic immune activation in HIV-1 infection [ 33 ], and microbial translocation especially LPS has been associated with HIV disease progression [ 34 , 35 ].

LPS treatment induced a rapid, transient increase in activated T cells. In our study, increased levels of LPS were associated with increased T cell activation and proliferation and increased production of HIV in LPS-treated animals, suggesting that LPS administration directly causes viral associated immune activation. The levels of B cells were downregulated after LPS administration in SHIV-infected monkeys in our study, and a few days later the cell number increased again, which is consistent with a previous report showing that LPS and HIV synergistically induce memory B cell apoptosis [ 36 ].

These results are consistent with the findings of Catalfamo et al. They have the potential to rapidly produce cytokines and eliminate infected cells [ 38 ]. PD-1 expression is associated with cytokine production as well as T cell expansion [ 44 ]. The cytokine-releasing capacity is also an important function of T cells against HIV infection.

In HIV-infected individuals, the presence of polyfunctional T cells has been associated with superior control of viral infection [ 46 , 47 ]. We showed here that the upregulation of PD-1 in T cells after LPS administration is associated with alterations in the distribution of T cell subpopulations and with impaired expression of cytokines. We reconfirmed the findings that PD-1 can be used as a marker for aberrant distribution of T cell subpopulations in HIV-1 infection [ 48 ]. A potential limitation of the present study is the smaller animal size. However, it is important to consider that the experiment was performed in a controlled system.

In summary, our data provided a direct relationship between LPS and immune activation. LPS can directly stimulate immune activation, making more target cells available for viral exploitation. Increased viral replication in target cells may in turn exacerbate these changes and result in an altered T cell homeostasis during chronic HIV infection. Muhammad Shahzad from Department of Pharmacology at University of Health Sciences, Lahore, for review of the paper, suggestions, and comments.

The funding agencies had no role in study design, data collection and analysis, decision to publish, or preparation of the paper. National Center for Biotechnology Information , U. Journal List J Immunol Res v. J Immunol Res. Published online Dec 2.

Author information Article notes Copyright and License information Disclaimer. Received Aug 10; Accepted Nov 5. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Immune activation plays a significant role in the disease progression of HIV. Introduction Chronic immune activation and inflammatory cytokine production are the hallmarks of HIV infection [ 1 , 2 ]. Materials and Methods 2. Absolute Quantification of Major Leukocyte Subpopulations Direct cell surface staining for whole blood and absolute number analysis were performed according to standard procedures and appropriate concentrations in this study.

Results 3. Open in a separate window. Figure 1. Figure 2. Figure 3. Figure 4. Figure 5. Figure 6. Figure 7. Discussion Persistent immune activation is a hallmark of progressive HIV infection. Disclaimer The funding agencies had no role in study design, data collection and analysis, decision to publish, or preparation of the paper.

Conflict of Interests The authors declare that they have no conflict of interests. References 1. Brenchley J.

1. Introduction

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HIV as a Cause of Immune Activation and Immunosenescence

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Microbial endocrinology: host–bacteria communication within the gut microbiome

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HIV as a Cause of Immune Activation and Immunosenescence

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Ginaldi L. Osteoporosis, inflammation and ageing. Immunity and Ageing. Crum-Cianflone N. Animals and infection. At the time of virus infection, therapy with sevelamer carbonate Renvela 2, mg, 3 times per day was initiated in 4 PTMs and was administered for 3 months. Remaining PTMs were used as untreated controls. During the follow-up, one of the PTMs in the study group died at day 53 after infection, due to causes unrelated to SIV infection or treatment. Sample collection. Blood was collected from all PTMs prior to infection, biweekly for 2 weeks, weekly for 4 weeks, and bimonthly thereafter.

Intestinal biopsies were collected prior to infection, during acute infection, at the set point, and during chronic infection, as described previously 11 , 28 , Samples were processed as described previously 11 , 28 , Laboratory assessment. Whole blood and mononuclear cells isolated from intestinal biopsies were analyzed by flow cytometry, as described previously 9. Plasma levels of LPS and sCD14 were measured as described previously 9 , 11 , to assess the levels of microbial translocation. Results were further confirmed by immunohistochemical staining for LPS, which was performed as described previously 18 on formalin-fixed, paraffin-embedded LNs collected prior to infection and at 2 time points during chronic infection Cytokine and chemokine testing and D-dimer testing were performed as previously described 9.

Differences in late temporal dynamics were analyzed using mixed-effects models, with each macaque as the grouping factor to account for the repeated measurements made in that animal. Models with fixed effects for time and treatment, with or without interactions, were tested. When an interaction was significant, we describe this difference in the text. Assumption on the distribution of residuals and appropriateness of the fitted values were checked by visual inspection of residual and fitted plots.

The best model for the data was chosen by comparing the log likelihood. All P values of less than 0. Study approval. We thank Jason Brenchley and Jake Estes for helpful discussion. Pandrea , R01 RR to C. Apetrei and I. Pandrea , 5P01 AI to A. Landay , and P30 AI to A. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. See the related article at Unraveling the relationship between microbial translocation and systemic immune activation in HIV infection.

Go to JCI Insight. Unraveling the relationship between microbial translocation and systemic immune activation in HIV infection. Liang Shan, Robert F. Siliciano Liang Shan, Robert F. Category: Commentary.

Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30) Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30)
Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30) Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30)
Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30) Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30)
Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30) Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30)
Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30) Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30)
Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30) Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30)
Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30) Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30)
Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30) Microbial Translocation Across the GI Tract (Annual Review of Immunology Book 30)

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