Does allergy impair innate immunity? Leads and lessons from atopic dermatitis

Abstract

To cite this article: Mrabet‐Dahbi S, Maurer M. Does allergy impair innate immunity? Leads and lessons from atopic dermatitis. Allergy 2010; 65: 1351–1356.AbstractHost defence responses against invading pathogens are well‐balanced, inflammatory processes of the innate and adaptive immune system. Impaired development or abnormal function of either system can result in failure to control pathogens and to clear infections. Infections have been claimed to modulate the onset and course of allergic diseases. This so‐called hygiene hypothesis is still an active area of research. In contrast, the effects of allergies on infections and pathogen‐directed immune responses are less well understood. Here, we have reviewed the existing evidence that allergies result in impaired innate immunity and we discuss recent observations that may explain why and how innate immunity is dysfunctional in allergic patients. With a focus on atopic dermatitis as a model of allergic disease, we speculate that one of the key features of allergic conditions, namely Th2 polarization, leads to several independent inhibitory effects on host defence and consequently to a higher risk of infections in allergic patients. A better understanding of impaired host defence and its mechanisms in allergic subjects will help to improve the management of these diseases.

Respiratory Infections in Adults with Atopic Disease and IgE Antibodies to Common Aeroallergens

“…The risk of LRTIs and URTIs was also related to atopic dermatitis and allergic rhinitis, although the 95% CI of the latter effect estimate included unity. It is known that atopic diseases share similar impaired immunological mechanisms that may increase susceptibility to respiratory infections [5], [19]. It is possible that dermatitis is a more consistent manifestation of atopic constitution and therefore the association with respiratory infections could be stronger compared to rhinitis.…”

“…Allergic patients typically present a Th2 polarization and hence it is suggested that the protective Th1 response is reduced. In addition, Th2-driven responses are believed to impair the innate immunity mediated host defense responses against microbial infections [5]. Th2-mediated cytokines, such as IL-4 and IL-13, induce airway inflammation that facilitates microbial attachment to the airway epithelia.…”

“…Atopic response is characterized by lymphocyte T-helper type 2 (Th2)-dependent immunological inflammation where Th2-derived cytokines, such as interleukin (IL) 4 and IL-13, induce allergic inflammation and the production of allergen-specific immunoglobulin E (IgE) antibodies [2]. As a consequence of Th2 polarization, Th1 response that plays an important role in protection against infectious agents mainly through Interferon gamma has been claimed to diminish in allergic individuals, leading to impairment of host defense responses against microbial infections [3]–[5]. Based on these mechanisms atopic subjects may have a higher susceptibility to respiratory infections than non-atopic subjects.…”

Polyunsaturated Fatty Acid-Derived Lipid Mediators and T Cell Function

“…(81)]. The regulation of Th2 cells by PGE 2 is likely to impact in Th2-mediated immune disorders such as atopic dermatitis and asthma (86, 87). Finally, when PGE 2 is produced by activated macrophages it reduces T cell activation and proliferation; this in turn leads to a reduction in cytokine production and consequent reduced stimulation of macrophages in a negative feed-back loop (72).…”

Update in clinical allergy and immunology

“…Recently, extracellular vesicles secreted by Staphylococcus aureus, which have been detected in skin of patients with AD, were shown to induce AD-like inflammation and causing a Th17-cell response in skin-draining lymph nodes in an animal model (86). Thus, Staphylococcus aureus might be involved in AD pathogenesis by secreting either extracellular vesicles that contain pathogenic proteins such as alpha-haemolysin and cysteine protease, or enterotoxins acting as superantigens and stimulating IgE responses, or both (87,88). The lack of antimicrobial peptide expression, for example human betadefensines and cathelicidine in AD skin, due to inhibitory effects of Th2 cytokines on keratinocytes, was shown to contribute to microbial infections observed in most patients with AD (89).…”