Absence of Interleukin-4 Determines Less Severe Pulmonary Paracoccidioidomycosis Associated with Impaired Th2 Response

Pina, Adriana; Valente-Ferreira, Rita C.; Molinari-Madlum, E. E. W. I.; Vaz, Celidéia Aparecida Coppi; Keller, Alexandre C.; Calich, Vera Lúcia Garcia

doi:10.1128/iai.72.4.2369-2378.2004

Cited by 43 publications

(34 citation statements)

References 53 publications

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“…These determinations coincided with the in situ description [29]. Similar results were described by Pina et al [55], who inoculated P. brasiliensis yeast cells in C57BL/6 mice and analysed the BAL fluid after infection. At 48 h post-challenge, they found an increase in the number of total cells, mainly due to PMN leukocytes influx in the BAL fluid.…”

Section: Inflammatory Cellssupporting

confidence: 88%

Pulmonary immune responses induced in BALB/c mice by Paracoccidioides brasiliensis conidia

2008

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Section: Inflammatory Cellssupporting

confidence: 88%

Pulmonary immune responses induced in BALB/c mice by Paracoccidioides brasiliensis conidia

2008

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“…Therefore, the absence of ICAM-1 significantly hampers the migration of cells toward the target tissue, which could lead to a reduction of the local production of factors that attract T cells, such as chemokines and cytokines, resulting in increased fungal load. The progression and dissemination of this infection is inversely correlated with the DTH response 13 and directly proportional with production of IL-4, 41 indicating, as shown before, 7,13,20 that the type-1 T-cell response is crucial to control the infection. Indeed, IL-4 is related with susceptibility and deficient formation of granulomas in P. brasiliensis-infected mice.…”

Section: Discussionsupporting

confidence: 62%

“…Indeed, IL-4 is related with susceptibility and deficient formation of granulomas in P. brasiliensis-infected mice. 41,42 Altogether, these findings suggest that the expression of ICAM-1 in the lungs of mice infected with P. brasiliensis contributes not only to the recruitment and adhesion of circulating T cells but also to the formation and organization of granulomas and with the adequate balance of cytokine production. Together these events orchestrate the generation of effector immune responses and the host defenses responsible for preventing the fungus to escape and disseminate.…”

Section: Discussionmentioning

confidence: 88%

Intercellular Adhesion Molecule-1 Is Required for the Early Formation of Granulomas and Participates in the Resistance of Mice to the Infection with the Fungus Paracoccidioides brasiliensis

Moreira

Campanelli

Cavassani

et al. 2006

The American Journal of Pathology

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The migration of leukocytes to inflammatory sites elicited by Paracoccidioides brasiliensis is supposed to be coordinated by cytokines and chemokines. Here, we investigated the role of intercellular adhesion molecule-1 (ICAM-1) in recruiting inflammatory cells to lungs of mice infected with P. brasiliensis and in determining the outcome of the disease. Expression of ICAM-1 was up-regulated on T lymphocytes after infection with the fungus, and its expression was dependent on interferon-␥, tumor necrosis factor-␣, and interleukin-12. Moreover, the absence of ICAM-1 resulted in high susceptibility to the infection and delayed formation of granulomatous lesions. In addition, the absence of ICAM-1 resulted in increased growth and dissemination of fungus , decreased number of CD3 ؉ CD4 ؉ and CD3 ؉ CD8 ؉ T cells , and increased production of interleukin-4 in the inflammatory site. The organization of a granulomatous reaction in mice deficient of ICAM-1 was delayed , starting only on day 60 after infection , whereas in wild-type mice it was complete on day 30 of infection. These data show that ICAM-1 is effectively involved in cellular migration and in the organization of the granulomatous lesion caused by the fungus P.

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“…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. Pulmonary fungal loads 2 weeks after infection were found to be decreased in IL-4 deficient mice when compared to normal wild-type mice (83).…”

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

confidence: 90%

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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Absence of Interleukin-4 Determines Less Severe Pulmonary Paracoccidioidomycosis Associated with Impaired Th2 Response

Cited by 43 publications

References 53 publications

Pulmonary immune responses induced in BALB/c mice by Paracoccidioides brasiliensis conidia

Pulmonary immune responses induced in BALB/c mice by Paracoccidioides brasiliensis conidia

Intercellular Adhesion Molecule-1 Is Required for the Early Formation of Granulomas and Participates in the Resistance of Mice to the Infection with the Fungus Paracoccidioides brasiliensis

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

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