IL‐4 depletion enhances host resistance and passive IgA protection against tuberculosis infection in BALB/c mice

Buccheri, Simona; Reljić, Rajko; Caccamo, Nadia; Iványi, Juraj; Singh, Mahavir; Salerno, Alfredo; Dieli, Francesco

doi:10.1002/eji.200636764

Cited by 57 publications

(43 citation statements)

References 55 publications

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“…Moreover, neutralization of IL-4 and IL-13 in AD skin augmented LL-37 and thereby limited viral infections (81). These findings are supported by murine studies showing that IL-4 depletion in BALB/c mice, which are commonly used to study allergic inflammation, substantially reduced Mycobacterium tuberculosis infections while reconstitution with IL-4 increased bacterial counts to wild-type levels (82). Moreover, another study demonstrated that alveolar macrophages from Paracoccidioides brasiliensis infected IL-4 )/) mice controlled in vitro fungal growth more efficiently than macrophages from wildtype mice and secreted higher levels of nitric oxide.…”

Section: Can Anti-th2 Intervention Strategies Restore Impaired Host Dmentioning

confidence: 80%

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

Mrabet-Dahbi

Maurer

2010

Allergy

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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.

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Section: Can Anti-th2 Intervention Strategies Restore Impaired Host Dmentioning

confidence: 80%

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

Mrabet-Dahbi

Maurer

2010

Allergy

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“…The extent by which the spontaneous post-chemotherapy relapse was prevented has been more profound than the previously reported CIT inhibition of fresh Mtb infection. 16 This could be due to differences between the persister or replicating target organisms. Furthermore, persisters arising rapidly following chemotherapy are apparently resilient to host T cell immunity, unlike the dormant organisms generated following acquired host T cell immunity.…”

Section: Discussionmentioning

confidence: 99%

“…13,14 This study has been initiated under the direct influence of our preceding experiments which showed, that (i) passive vaccination with a mouse IgA monoclonal antibody (mAb) against the a-crystallin (Acr) antigen of Mtb together with IFNg reduced the lung infection and pathology in BALB/c mice 15 and (ii) combining this regimen with the inoculation of IL-4 neutralizing antibody was even more protective. 16 The combined immunotherapy regimen composed of IFNg þ IgA þ anti-IL-4 was evaluated in this study for its capacity to reduce the spontaneous relapse of active tuberculous infection following short-term (incomplete) chemotherapy.…”

Section: Introductionmentioning

confidence: 99%

Prevention of the post-chemotherapy relapse of tuberculous infection by combined immunotherapy

Buccheri¹,

Reljić²,

Caccamo³

et al. 2009

Tuberculosis

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s u m m a r yWe report that a recently developed combined immunotherapy (CIT) has the capacity to prevent a spontaneous relapse of replicating Mycobacterium tuberculosis bacilli in the lungs of BALB/c, C57Bl/6 or C3H/HeJ strains of mice, following 4 weeks of non-sterilising treatment with isoniazid and rifampicin. The CIT regimen, represented by recombinant IFNg, anti-a crystalline monoclonal IgA antibody and IL-4 neutralizing polyclonal antibody, reduced the 8-week relapse of viable bacterial counts in the lungs most significantly, when CIT was inoculated during the 5th week post infection, i.e. during the 3rd week of chemotherapy. Although CIT enhanced lung granuloma area, nitric oxide, cytokine and chemokine levels in lung washings significantly, these could not be directly associated with the beneficial effect of CIT on the degree of relapse in the lungs. These results represent a proof-of-principle, that the described CIT, when combined with chemotherapy, could have potential for future development of a shorter regimen of tuberculosis treatment.

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“…In genetically deficient IL-4-/-BALB/c mice, infection in both lungs and spleen was substantially reduced for up to 8 weeks. Reconstitution of IL-4-/-mice with rIL-4 increased bacterial counts to wild-type levels and making mice refractory to protection by IgA/IFN- [65].…”

Section: Studies Performed With Monoclonal Antibodiesmentioning

confidence: 99%