ReviewAlcohol and inflammation and immune responses: Summary of the 2005 Alcohol and Immunology Research Interest Group (AIRIG) meeting
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.
References (26)
- et al.
T-cell activation after chronic ethanol ingestion in mice
Alcohol
(2004) - et al.
Ethanol alters cellular activation and CD14 partitioning in lipid rafts
Biochem Biophys Res Commun
(2005) - et al.
Alcohol, injury, and cellular immunity
Alcohol
(2002) - et al.
Modulation of perforin, granzyme A, and granzyme B in murine natural killer (NK), IL2 stimulated NK, and lymphokine-activated killer cells by alcohol consumption
Cell Immunol
(1999) - et al.
Chronic ethanol ingestion by mice increases expression of CD80 and CD86 by activated macrophages
Alcohol
(2004) - et al.
Suppression of the granulocyte colony-stimulating factor response to Escherichia coli challenge by alcohol intoxication
Alcohol Clin Exp Res
(1998) - et al.
Alcohol-induced suppression of lung chemokine production and the host defense response to Streptococcus pneumoniae
Alcohol Clin Exp Res
(2003) - et al.
The effects of binge alcohol exposure on bone resorption and biomechanical and structural properties are offset by concurrent bisphosphonate treatment
Alcohol Clin Exp Res
(2004) Alcohol abuse, alcoholism, and damage to the immune system—a review
Alcohol Clin Exp Res
(1998)- et al.
Modulation of T-cell adhesion markers, and the CD45R and CD57 antigens in human alcoholics
Alcohol Clin Exp Res
(1995)
Alcohol ingestion impairs host defenses predisposing otherwise healthy mice to Pneumocystis carinii infection
Alcohol Clin Exp Res
Effect of acute ethanol exposure on the dermal inflammatory response after burn injury
Alcohol Clin Exp Res
In vivo ethanol exposure down-regulates TLR2-, TLR4-, and TLR9-mediated macrophage inflammatory response by limiting p38 and ERK1/2 activation
J Immunol
Cited by (32)
Lifestyle, Hormonal, and Metabolic Environmental Risks for Rheumatoid Arthritis
2022, Rheumatic Disease Clinics of North AmericaPotential of Lifestyle Changes for Reducing the Risk of Developing Rheumatoid Arthritis: Is an Ounce of Prevention Worth a Pound of Cure?
2019, Clinical TherapeuticsCitation Excerpt :There is evidence that moderate alcohol intake may reduce RA risk compared with lower levels of alcohol consumption. The mechanism behind this association109 may be through downregulation of the immune response110 and decreased production of pro-inflammatory cytokines.95,111,112 However, alcohol consumption might be indicative of overall health status and be a confounding effect because those who abstain completely may be experiencing chronic illness, have previously been heavy drinkers, or pre-cursor symptoms before RA may have influenced drinking behaviors (reverse causation).110
Crocin may be useful to prevent or treatment of alcohol induced neurodegeneration and neurobehavioral sequels via modulation of CREB/BDNF and Akt/GSK signaling pathway
2019, Medical HypothesesCitation Excerpt :Conferring to these data, it appears that part of the damaging effects of alcohol is mediated via mitochondrial dysfunction and disturbance in oxidative and antioxidant balances [50,51]. It was demonstrated that chronic administration of alcohol significantly rises the level of pro-inflammatory cytokines like IL-β and TNF-α in the brain tissue [51]. Previous works which have stated the increase of pro-inflammatory cytokines following alcohol and other similar agents’ abuse [51].
Protection of resveratrol and its analogues against ethanol-induced oxidative DNA damage in human peripheral lymphocytes
2011, Mutation Research - Genetic Toxicology and Environmental MutagenesisCitation Excerpt :Diseases related to ethanol abuse are becoming one of the most costly health problems in the world [1]. Binge drinking, a commonly occurring pattern of ethanol abuse, induces severe genotoxicity that plays a core role in the diseases related to ethanol abuse [2,3]. We have previously proved, for the first time, ethanol in the blood concentration under binge drinking condition induces oxidative DNA damage in human peripheral lymphocytes in vitro.
Phytochemicals from medicinal plants from African forests with potentials in rheumatoid arthritis management
2022, Journal of Pharmacy and Pharmacology