A comparison of cytokine responses in respiratory syncytial virus and influenza A infections in infants

Sung, Rita Yn Tz; Hui, Shuk Yi Annie; Wong, Chun Kwok; Lam, Christopher Wai Kei; Yin, Jun

doi:10.1007/s004310000676

Cited by 79 publications

(67 citation statements)

References 15 publications

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“…Our data enhance earlier findings with isolated cell types in vitro (21,23) and confirm and extend these earlier results. Furthermore, the observation that LXA 4 and the 15-epi-LXA 4 are potent inhibitors of RANTES release is an important addition to the bioactivity profile of these compounds and suggests a role for LXs as potential therapeutic modifiers of other diseases in which RANTES dysregulation plays an important role, such as allograft rejection (43), atopy (44), and viral infections (45). The net effect of LX-mediated attenuation of neutrophil adherence and chemokine production may translate into a reduction in the recruitment of inflammatory cells and downregulation of intestinal inflammation.…”

Section: Discussionmentioning

confidence: 99%

Lipoxin A4 and Aspirin-Triggered 15-Epi-Lipoxin A4 Antagonize TNF-α-Stimulated Neutrophil-Enterocyte Interactions In Vitro and Attenuate TNF-α-Induced Chemokine Release and Colonocyte Apoptosis in Human Intestinal Mucosa Ex Vivo

Goh

Baird

O’Keane

et al. 2001

The Journal of Immunology

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Lipoxins (LXs) are lipoxygenase-derived eicosanoids and putative endogenous braking signals for inflammation in the gastrointestinal tract and other organs. Aspirin triggers the production of 15-epimers during cell-cell interaction in a cytokine-primed milieu, and aspirin-triggered 15-epi-5(S),6(R),15(S)-trihydroxy-7,9,13-trans-11-cis-eicosatetraenoic acid (15-epi-LXA4) may contribute to the bioactivity profile of this prototype nonsteroidal anti-inflammatory drug in vivo. We determined the effect of LXA4, 15-(R/S)-methyl-11,12-dehydro-LXA4 methyl ester (15-(R/S)-methyl-LXA4), and stable analogs of LXA4 on TNF-α-stimulated neutrophil-enterocyte interaction in vitro and TNF-α-stimulated chemokine release, changes in mucosal architecture, and enterocyte apoptosis in cytokine-activated intact human colonic mucosa ex vivo. LXA4, 15-(R/S)-epi-LXA4, and 16-phenoxy-11,12-dehydro-17,18,19,20-tetranor-LXA4 methyl ester (16-phenoxy-LXA4) inhibited TNF-α-stimulated neutrophil adherence to epithelial monolayers at nanomolar concentrations. In parallel experiments involving human colonic mucosa ex vivo, LXA4potently attenuated TNF-α-stimulated release of the C-X-C chemokine IL-8, and the C-C chemokines monocyte-chemoattractant protein-1 (MCP-1) and RANTES. Exposure of strips of normal human colonic mucosa to TNF-α induced disruption of mucosa architecture and enhanced colonocyte apoptosis via a caspase-3-independent mechanism. Prior exposure of the mucosa strips to 15-(R/S)-methyl-LXA4 attenuated TNF-α-stimulated colonocyte apoptosis and protected the mucosa against TNF-α-induced mucosal damage. In aggregate, our data demonstrate that lipoxins and aspirin-triggered 15-epi-LXA4 are potent antagonists of TNF-α-mediated neutrophil-enterocyte interactions in vitro, attenuate TNF-α-triggered chemokine release and colonocyte apoptosis, and are protective against TNF-α-induced morphological disruption in human colonic strips ex vivo. Our observations further expand the anti-inflammatory profile of these lipoxygenase-derived eicosanoids and suggest new therapeutic approaches for the treatment of inflammatory bowel disease.

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Section: Discussionmentioning

confidence: 99%

Lipoxin A4 and Aspirin-Triggered 15-Epi-Lipoxin A4 Antagonize TNF-α-Stimulated Neutrophil-Enterocyte Interactions In Vitro and Attenuate TNF-α-Induced Chemokine Release and Colonocyte Apoptosis in Human Intestinal Mucosa Ex Vivo

Goh

Baird

O’Keane

et al. 2001

The Journal of Immunology

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“…Eosinophils are recruited by Th2 or inflammatory chemoattractants, including IL-5, eotaxin/CCL11, and RANTES, and are activated to release cytotoxic proteins and antiviral RNase as well as Th2 cytokines and inflammatory chemokines and cytokines. However, the prevalence of eosinophils among airway leukocytes from RSV-infected infants, 1 to 3%, was low and approximately the same as for influenza virus, and thus does not seem to represent a prominent or unique feature of RSV pathogenesis (101,143). Furthermore, the net effects of eosinophils are not necessarily pathogenic: hypereosinophilia in a transgenic mouse that overexpresses IL-5 was associated with protective and disease-sparing effects against RSV rather than increased disease (118).…”

Section: Protective and Pathogenic Features Of The Host Responsementioning

confidence: 93%

“…Clinical studies have documented increased expression of inflammatory mediators or their mRNAs in respiratory secretions of infants and children hospitalized for RSV disease compared to controls, including IL-6, tumor necrosis factor ␣, IL-8, RANTES, macrophage inflammatory protein 1␣/CCL3, eotaxin, and monocyte chemotactic protein 1/CCL2, among others (47,64,100). As is typical for acute inflammation, neutrophils are the predominant airway leukocyte in infants with RSV bronchiolitis, accounting for 84% or more of the cells, compared to 66% for influenza virus (101,143). IL-8 is the major chemoattractant for neutrophils.…”

Section: Protective and Pathogenic Features Of The Host Responsementioning

confidence: 99%

Viral and Host Factors in Human Respiratory Syncytial Virus Pathogenesis

Collins¹,

Graham

2008

J Virol

427

478

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Human respiratory syncytial virus (RSV) was first isolated in 1956 from a laboratory chimpanzee with upper respiratory tract disease (for general reviews, see references 21, 57, 102, and 145). RSV was quickly determined to be of human origin and was shown to be the leading worldwide viral agent of serious pediatric respiratory tract disease. In a 13-year prospective study of infants and children in the United States, RSV was detected in 43%, 25%, 11%, and 10% of pediatric hospitalizations for bronchiolitis, pneumonia, bronchitis, and croup, respectively (110). Approximately two-thirds of infants are infected with RSV during the first year of life, and 90% have been infected one or more times by 2 years of age. The rate of hospitalization for primary infection is approximately 0.5% but can vary by situation and ethnic group and can be as high as 25% (77).RSV also is a significant cause of morbidity and mortality in the elderly, with an impact approaching that of nonpandemic influenza virus (39). RSV readily infects severely immunocompromised individuals, most notably allogeneic bone marrow transplant recipients, causing high mortality. RSV also makes a substantial contribution to upper respiratory tract disease in individuals of all ages (59,65 Although RSV has a single serotype, reinfection can occur throughout life. RSV in yearly winter/early spring epidemics in temperate regions; elsewhere, the timing of RSV activity can vary widely with the locale. The RSV reservoir in the offseason is unknown. Strains circulate quickly around the earth (150). Neither a vaccine nor an effective antiviral therapy is available, although there is active research in both areas (23,78,138). However, infants at high risk for serious disease can receive passive immunoprophylaxis during the epidemic season by a monthly injection of a commercial RSV-neutralizing monoclonal antibody, palivizumab (Synagis), which provides a 55% reduction in RSV-associated hospitalization (17). THE VIRUSRSV (family Paramyxoviridae, order Mononegavirales) is an enveloped virus with a single-stranded negative-sense RNA genome of 15.2 kb (21). There are animal versions of RSV, including bovine RSV (BRSV) and pneumonia virus of mice (PVM), suggesting that species jumping occurred during the evolution of these viruses. However, there is no animal reservoir for human RSV.Efficient infection by RSV of established cell lines in vitro involves binding to cell-surface glycosaminoglycans (62). However, it is not known how closely this binding models attachment in vivo or whether it is an initial interaction that is followed by a second, higher-affinity step that remains to be identified. The nucleocapsid gains entry to the cytoplasm by membrane fusion; surprisingly, this may involve clathrin-mediated endocytosis rather than surface fusion typical of paramyxoviruses (85). Viral gene expression and RNA replication occur in the cytoplasm, and virions acquire a lipid envelope by budding through the plasmid membrane (Fig. 1). Virions are pleomorphic and include spheres ...

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“…75,76 2) a deficient anti-viral T H 1 response and 3) a low secretion of IFN-g and TNF-a in peripheral blood mononuclear cells 77 and in nasopharyngeal aspirates, 78 respectively. Nevertheless, hRSV-infected infants suffering from bronchiolitis present higher levels of TNF-a in BALF at day 1 of intubation, as compared with controls.…”

Section: An Adequate Cd4mentioning

confidence: 99%

Aberrant T cell immunity triggered by human Respiratory Syncytial Virus and human Metapneumovirus infection

et al. 2016

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Human Respiratory syncytial virus (hRSV) and human metapneumovirus (hMPV) are the two major etiological viral agents of lower respiratory tract diseases, affecting mainly infants, young children and the elderly. Although the infection of both viruses trigger an antiviral immune response that mediate viral clearance and disease resolution in immunocompetent individuals, the promotion of long-term immunity appears to be deficient and reinfection are common throughout life. A possible explanation for this phenomenon is that hRSV and hMPV, can induce aberrant T cell responses, which leads to exacerbated lung inflammation and poor T and B cell memory immunity. The modulation of immune response exerted by both viruses include different strategies such as, impairment of immunological synapse mediated by viral proteins or soluble factors, and the induction of pro-inflammatory cytokines by epithelial cells, among others. All these viral strategies contribute to the alteration of the adaptive immunity in order to increase the susceptibility to reinfections.In this review, we discuss current research related to the mechanisms underlying the impairment of T and B cell immune responses induced by hRSV and hMPV infection. In addition, we described the role each virulence factor involved in immune modulation caused by these viruses.

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A comparison of cytokine responses in respiratory syncytial virus and influenza A infections in infants

Cited by 79 publications

References 15 publications

Lipoxin A4 and Aspirin-Triggered 15-Epi-Lipoxin A4 Antagonize TNF-α-Stimulated Neutrophil-Enterocyte Interactions In Vitro and Attenuate TNF-α-Induced Chemokine Release and Colonocyte Apoptosis in Human Intestinal Mucosa Ex Vivo

Lipoxin A4 and Aspirin-Triggered 15-Epi-Lipoxin A4 Antagonize TNF-α-Stimulated Neutrophil-Enterocyte Interactions In Vitro and Attenuate TNF-α-Induced Chemokine Release and Colonocyte Apoptosis in Human Intestinal Mucosa Ex Vivo

Viral and Host Factors in Human Respiratory Syncytial Virus Pathogenesis

Aberrant T cell immunity triggered by human Respiratory Syncytial Virus and human Metapneumovirus infection

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