Elsevier

Alcohol

Volume 38, Issue 2, February 2006, Pages 121-125
Alcohol

Review
Alcohol and inflammation and immune responses: Summary of the 2005 Alcohol and Immunology Research Interest Group (AIRIG) meeting

https://doi.org/10.1016/j.alcohol.2006.05.001Get rights and content

Abstract

The 10th annual meeting of the Alcohol and Immunology Research Interest Group (AIRIG) was held at Loyola University Medical Center, Maywood, Illinois on November 18, 2005. The AIRIG meeting was held to exchange new findings and ideas regarding the profound suppressive effects of alcohol exposure on the immune system. The event consisted of five sessions, two of which featured plenary talks from invited speakers, two with oral presentations from selected abstracts, and a final poster session. Participants presented a range of novel information focused on ethanol-induced effects on innate and adaptive immunity after either acute or chronic exposure. In particular, participants offered insights into the negative effects of ethanol on the innate processes of adhesion, migration, inflammation, wound repair, and bone remodeling. Presentations also focused on the means by which ethanol disrupts activation of macrophages and dendritic cells (DC), especially stimulation mediated by Toll-like receptor ligands. Additional talks provided new data on the means by which ethanol suppresses adaptive immunity, with an emphasis on DC-mediated activation of T cells, effector T cell activity, and T cell-driven B cell responses.

Introduction

It is increasingly clear that alcohol abuse has a major impact on both the innate and adaptive arms of the immune response. The innate immune system is designed to prevent colonization of tissues by pathogens and consists of granulocytes, monocytes/macrophages, and natural killer cells. Adaptive immunity is focused on eliminating organisms that have penetrated sterile portions of the body, and uses B cells and T cells that have been alerted to the presence of pathogens by dendritic cells (DC). Ethanol-induced dysfunction within the immune system has a range of deleterious effects on human health, including major elevations in the rates of infectious disease (Cook, 1998, Happel and Nelson, 2005, MacGregor and Louria, 1997, Nelson and Kolls, 2002, Szabo, 1999). Investigators are not only making progress documenting the nature and range of immune lesions, but are also beginning to identify the means by which ethanol exposure leads to impairment. This is particularly true with innate immunity, where current research is leading to a better understanding of alcohol-induced dysfunction in granulocytes, macrophages, and DC as well as innate processes such as leukocyte–endothelial interactions, inflammation, and tissue remodeling (Happel and Nelson, 2005, Messingham et al., 2002, Nagy, 2003).

Although it is well understood that long-term alcohol abuse severely damages immune function, the field of alcohol research has gained an appreciation that acute ethanol exposure in the form of binge drinking can also compromise protective immunity (Bagby et al., 1998, Boe et al., 2003, D'Souza et al., 1995, Faunce et al., 2003). However, the means by which acute and chronic ethanol exposure disrupt the immune system are likely to differ, with acute or binge drinking having a prominent effect on innate immunity and long-term intake leading to alterations in both the innate and adaptive systems. As such, greater attention is being given to the development and characterization of animal models that mimic acute versus chronic alcohol abuse. Using these models, researchers in the field are becoming better equipped to approach mechanistic questions.

To further explore these issues, the 10th meeting of the Alcohol and Immunology Research Interest Group (AIRIG) was held at Loyola University Medical Center on November 18, 2005. The meeting was supported by an R13 grant from the National Institute on Alcohol Abuse and Alcoholism (AA016057) and by funds from the Department of Surgery at Loyola University Medical Center. The meeting was organized by Dr. Elizabeth J. Kovacs and Dr. Luisa A. DiPietro (Loyola University Medical Center), Dr. Lou Ann S. Brown (Emory University School of Medicine), Dr. Robert T. Cook (University of Iowa College of Medicine), and Dr. Thomas R. Jerrells (University of Nebraska Medical Center). The day consisted of five sessions, two of which featured invited speakers and two structured around short presentations of selected abstracts, as well as a poster session. Abstracts for all oral and poster presentations were previously published in this journal (Alcohol 36, 127–135).

Section snippets

Alcohol and inflammation

The first plenary session, chaired by Dr. Lou Ann Brown, focused on the effects of ethanol in innate immunity and inflammation. Dr. Luisa DiPietro detailed the effects of prior ethanol exposure on dermal wound healing using both in vivo and in vitro systems. Using animal models, previous work from Dr. DiPietro and colleagues demonstrated a delay in wound healing after ethanol exposure, with a decrease in both wound collagen content and vascularity (Radek et al., 2005). Dr. DiPietro presented

Alcohol and immunity

The second plenary session was chaired by Dr. DiPietro, and centered on the effects of ethanol on induction and maintenance of adaptive immunity. Dr. Pranoti Mandrekar of the University of Massachusetts Medical Center discussed how acute ethanol exposure affects the ability of myeloid-derived DC to activate T cells (Mandrekar et al., 2004). In this study, the investigators used two methods to obtain ethanol-exposed myeloid-derived DC. In the first (in vitro exposure), peripheral blood monocytes

Short presentations

As a complement to the plenary speakers, two sessions were organized to feature podium presentations selected from a number of abstracts submitted by meeting participants. As with the plenary sessions, these presentations covered a range of topics and focused on both innate and adaptive immunity. Dr. Pratibha Joshi from Emory University led off a number of talks on innate immunity and discussed work in the rat showing a negative effect of chronic ethanol intake on GM-CSF receptor expression on

Acknowledgments

The authors and participants gratefully acknowledge financial support for the 2005 AIRIG meeting from the NIAAA (AA016057) and Department of Surgery, Loyola Medical Center. The administrative and logistic support provided by Letta Kochalis is also greatly appreciated.

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