Innate immune mechanism in allergic asthma

Suarez, Carlos J.; Parker, Nathan J.; Finn, Patricia W.

doi:10.1007/s11882-008-0085-8

Cited by 34 publications

(27 citation statements)

References 70 publications

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“…For example, M1 responses, important in mediating resistance against acute viral and mycobacterial infections, may also contribute to the induction of autoimmune diseases such as rheumatoid arthritis and multiple sclerosis [56 -59]. Alternatively, M2 polarization, important in controlling helminthic infections, has been linked to the development and persistence of asthma and allergic diseases [60,61]. Interestingly, TAM, including tyrosine kinase with Ig-like and EGF-like domains 2 (Tie2)-derived macrophages [62,63], closely resembles M2 macrophages when analyzed for function and transcriptome expression [64,65].…”

Section: Polarization Of Human Macrophages Along M1 and M2 Pathwaysmentioning

confidence: 99%

Macrophage polarization and HIV-1 infection

Cassol

Cassetta

Alfano

et al. 2009

Journal of Leukocyte Biology

137

144

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Polarization of MP into classically activated (M1) and alternatively activated (M2a, M2b, and M2c) macrophages is critical in mediating an effective immune response against invading pathogens. However, several pathogens use these activation pathways to facilitate dissemination and pathogenesis. Viruses generally induce an M1-like phenotype during the acute phase of infection. In addition to promoting the development of Th1 responses and IFN production, M1 macrophages often produce cytokines that drive viral replication and tissue damage. As shown for HIV-1, polarization can also alter macrophage susceptibility to infection. In vitro polarization into M1 cells prevents HIV-1 infection, and M2a polarization inhibits viral replication at a post-integration level. M2a cells also express high levels of C-type lectins that can facilitate macrophage-mediated transmission of HIV-1 to CD4(+) T cells. Macrophages are particularly abundant in mucosal membranes and unlike DCs, do not usually migrate to distal tissues. As a result, macrophages are likely to contribute to HIV-1 pathogenesis in mucosal rather than lymphatic tissues. In vivo polarization of MP is likely to span a spectrum of activation phenotypes that may change the permissivity to and alter the outcome of HIV-1 and other viral infections.

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Section: Polarization Of Human Macrophages Along M1 and M2 Pathwaysmentioning

confidence: 99%

Macrophage polarization and HIV-1 infection

Cassol

Cassetta

Alfano

et al. 2009

Journal of Leukocyte Biology

137

144

View full text Add to dashboard Cite

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“…Perinatal stress may influence the evolving systemic propensity for type Th2 responses (i.e., enhanced adaptive immunity)8. Antigen-independent responses including innate immune cells (e.g., bronchial epithelial cells, alveolar macrophages, and dendritic cells) may also be important in modifying airway inflammation 59. Factors, including stress, that slow maturation of local immune networks (e.g., dendritic cells [DCs], epithelial cells [ECs], regulatory T cells) may predispose to a Th2 phenotype 60.…”

Section: Examples From Leading Pediatric Developmental Disordersmentioning

confidence: 99%

Moving towards making social toxins mainstream in children's environmental health

Wright

2009

Current Opinion in Pediatrics

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Purpose of Review-While traditional disciplinary research theory and methods have focused separately on how social and physical environmental factors affect children's health, evolving research underscores important integrated effects.Recent findings-This review outlines the specific reasons why social determinants should be considered mainstream in children's environmental health research with particular focus on interactive effects between social and physical hazards. These include (a) sensitivity of overlapping physiological systems, via epigenesis, programming, and plasticity to social and physical environmental moderation that may impact health across the life span; (b) ways in which social environmental vulnerabilities moderate the effects of physical environmental factors providing specific examples related to respiratory health and neurodevelopment; (c) overlapping exposure distribution profiles; and (d) relevance to pediatric health disparities.Summary-Because of the covariance across exposures and evidence that social stress and other environmental toxins (e.g., pollutants, tobacco smoke) may influence common physiological pathways (e.g., oxidative stress, pro-inflammatory immune pathways, autonomic disruption), understanding the potential synergistic effects promises to more completely inform children's environmental health risk. While this discussion focuses around the respiratory and neurological systems, these concepts extend more broadly to children's psychological and physical development.

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“…Asthma is believed to be driven by inappropriate Th2-dominated immune responses to environmental allergens (3–6). In addition, the role of innate immunity in asthma has also attracted interest of investigators (7–10). Complement is a key component of the host innate immunity, and previous clinical and laboratory studies have suggested an important role of the complement system in this disease (11–20).…”

Section: Introductionmentioning

confidence: 99%

Properdin Contributes to Allergic Airway Inflammation through Local C3a Generation

Wang

Miwa

Ducka-Kokalari

et al. 2015

The Journal of Immunology

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Complement is implicated in asthma pathogenesis but its mechanism of action in this disease remains incompletely understood. Here we studied the role of properdin (P), a positive alternative pathway complement regulator, in allergen-induced airway inflammation. Allergen challenge stimulated P release into the airways of asthmatic patients and P levels positively correlated with proinflammatory cytokines in human bronchoalveolar lavage (BAL). High levels of P were also detected in the BAL of OVA-sensitized and challenged but not naïve mice. Compared with wild-type mice, P-deficient (P−/−) mice had markedly reduced total and eosinophil cell counts in BAL and significantly attenuated airway hyperresponsiveness to methacholine. Antibody blocking of P at both sensitization and challenge phases or at challenge phase alone, but not at sensitization phase alone, reduced airway inflammation. Conversely, intranasal reconstitution of P to P−/− mice at the challenge phase restored airway inflammation to wild-type levels. Notably, C3a levels in the BAL of OVA-challenged P−/− mice were significantly lower than in wild-type mice, and intranasal co-administration of an anti-C3a mAb with P to P−/− mice prevented restoration of airway inflammation. These results show that P plays a key role in allergen-induced airway inflammation and represents a potential therapeutic target for human asthma.

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Innate immune mechanism in allergic asthma

Cited by 34 publications

References 70 publications

Macrophage polarization and HIV-1 infection

Macrophage polarization and HIV-1 infection

Moving towards making social toxins mainstream in children's environmental health

Properdin Contributes to Allergic Airway Inflammation through Local C3a Generation

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