Signals of Th2 immune response from COVID-19 patients requiring intensive care

Roncati, Luca; Nasillo, Vincenzo; Lusenti, Beatrice; Riva, Giovanni

doi:10.1007/s00277-020-04066-7

“…Recent studies demonstrate that In uenza A variants can trigger the more severe neutrophilic response that appears to be determinant of the severity of lung injury and the tragic outcomes. It also has shown that these cytokines and neutrophils chemoattraction may be associated with the pathogenesis of respiratory diseases by exacerbating the in ammatory response [17,22]. In our study, the COVID-19 lower tissue expression of IL-17A and IL-8 accompanied by lower neutrophil score may demonstrate that the SARS-CoV-2 in ammatory response's pathogenesis differs from that observed in the H1N1pdm09 disease [23].…”

Section: Discussionmentioning

confidence: 44%

“…A recent study described that, although out of the expected patterns of viral lung infection, patients with COVID-19 showed an increased Th2 response. The innate and Th1 responses, mediated by macrophages, neutrophils, and T lymphocytes, are known to be more effective in controlling the viral infection, but for reasons that are still unclear, this process seems to be inhibited in SARS-CoV-2 infection [17]. The innate and adaptive Th1 response modulation occurs due to the presence of viral proteins and the consequent activation of TCD8+ lymphocytes, which are remarkably reduced in infection by SARS-CoV-2.…”

Section: Discussionmentioning

confidence: 99%

“…The innate and adaptive Th1 response modulation occurs due to the presence of viral proteins and the consequent activation of TCD8+ lymphocytes, which are remarkably reduced in infection by SARS-CoV-2. Another current work dedicated to SARS-CoV-2, reported the possible evasion of the immune system by the virus, explained by the increased incubation time, in comparison with viruses such as In uenza [17,18,19].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Alveolar Neutrophilic Recruitment in COVID-19 May Not be Mediated by Th17 Response

Azevedo

¹

,

Paula

²

,

Nagashima

³

et al. 2020

Preprint

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Introduction: The COVID-19 current pandemic disease differs from the H1N1pdm09 caused by Influenza A virus H1N1 subtype, by how it induces a pro-inflammatory response in infected lungs. Objective: Investigate the role of Th17 response in the pathogenesis of COVID-19 injury by analyzing the tissue expression of interleukins 8 and 17A and the neutrophils in lung samples of patients who die of COVID-19, comparing to H1N1pdm09. Study design and post-mortem results: Six lung samples from patients SARS-CoV-2 infected (COVID-19 group), and ten lung samples from adults who died from H1N1pdm09 (H1N1 group), were tested. A control group was also added to the study. H&E slides were used for neutrophils scoring. The tissue expression of IL-8 and IL-17A was identified by immunohistochemistry. Tissue expression increasing of IL-17A and IL-8 and a higher number of neutrophils were identified in samples from the H1N1 group when compared to the COVID-19 group. Discussion: It is suggested that the SARS-CoV-2 virus evokes an exacerbated response of the host's immune system but differs from that observed in the H1N1pdm09 disease because it may not be trigger by Th17 response. With the low expression of IL-8, IL-17A, neutrophil recruitment to the site of infection becomes impaired, resulting in viral persistence. On the other hand, in the COVID-19 disease, the immune response by Th2 cells seems to be exacerbated, observed by the extent of the lung injury. This uncontrolled response and, mainly, the lack of a therapeutic target, culminates in disease progression and, consequently, in shorter survival time.

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“…What is more, the signi cantly decreased B cell in severe COVID-19 patents indicated that humoral immunity has been attenuated in antiviral response of SARS-CoV-2. It has reported [23][24][25] that T-helper type 1 (Th1), T-helper type 2 (Th2), and regulatory T cells were varying degrees of activated in peripheral blood from critical COVID-19 patients after stimulation with speci c antigen of SARS-CoV-2. It can be speculated all the CD4+ T cell subgroups were exhaust in blood of critical COVID-19 patients for the severely damaged lymphoid organs and/or exudation of circulating lymphocytes into lung [9] , although the alteration of CD4+ T cell subsets warrants further investigation.…”

Section: Discussionmentioning

confidence: 99%

Lymphocyte subset alterations with disease severity, imaging manifestation, and delayed hospitalization in COVID-19 patients

Wu

¹

,

Wu

²

,

Huang

³

et al. 2020

Preprint

0

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Background: COVID-19 continuously threated public health heavily. Present study aimed to investigate the lymphocyte subset alterations with disease severity, imaging manifestation, and delayed hospitalization in COVID-19 patients.Methods: Lymphocyte subsets was classified using flow cytometry with peripheral blood collected from 106 patients.Results: Multivariate logistic regression showed that chest tightness, lymphocyte count, and γ-glutamyl transpeptidase were the independent predictors for severe COVID-19. The T cell, CD4+ T cell and B cell counts in severe patients were significantly lower than that in mild patients (p = 0.004, 0.003 and 0.046, respectively). Only the T cell count was gradually decreased with the increase of infiltrated quadrants of lesions in computed tomography (CT) (p = 0.043). The T cell, CD4+ T cell, and CD8+ T cell counts were gradually decreased with the increase of infiltrated area of the maximum lesion in CT (p = 0.002, 0.003, 0.028; respectively). The T cell count, as well as CD4+ T cell, CD8+ T cell, and NK cell counts were gradually decreased with the increased delayed hospitalization (p = 0.003, 0.002, 0.013, and 0.012; respectively). The proportion of T cell was gradually decreased but B cell was gradually increased with the increased delayed hospitalization (p = 0.031 and 0.003, respectively).Conclusion: T cell and CD4+ T cell counts negatively correlated with disease severity, CT manifestation and delayed hospitalization. CD4+ T cell was mainstay of immunity response in COVID-19 patients.

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“…What is more, the signi cantly decreased B cell in severe COVID-19 patents indicated that humoral immunity has been attenuated in antiviral response of SARS-CoV-2. It has reported [24][25][26] that T-helper type 1 (Th1), T-helper type 2 (Th2), and regulatory T cells were varying degrees of activated in peripheral blood from critical COVID-19 patients after stimulation with speci c antigen of SARS-CoV-2. It can be speculated all the CD4 + T cell subgroups were exhaust in blood of critical COVID-19 patients for the severely damaged lymphoid organs and/or exudation of circulating lymphocytes into lung [9] , although the alteration of CD4+ T cell subsets warrants further investigation.…”

Section: Discussionmentioning

confidence: 99%

Lymphocyte subset alterations with disease severity, imaging manifestation, and delayed hospitalization in COVID-19 patients

Wu

¹

,

Wu

²

,

Huang

³

et al. 2020

Preprint

0

View full text Add to dashboard Cite

Background: COVID-19 continuously threated public health heavily. Present study aimed to investigate the lymphocyte subset alterations with disease severity, imaging manifestation, and delayed hospitalization in COVID-19 patients.Methods: Lymphocyte subsets was classified using flow cytometry with peripheral blood collected from 106 patients.Results: Multivariate logistic regression showed that chest tightness, lymphocyte count, and γ-glutamyl transpeptidase were the independent predictors for severe COVID-19. The T cell, CD4+ T cell and B cell counts in severe patients were significantly lower than that in mild patients (p = 0.004, 0.003 and 0.046, respectively). Only the T cell count was gradually decreased with the increase of infiltrated quadrants of lesions in computed tomography (CT) (p = 0.043). The T cell, CD4+ T cell, and CD8+ T cell counts were gradually decreased with the increase of infiltrated area of the maximum lesion in CT (p = 0.002, 0.003, 0.028; respectively). The T cell count, as well as CD4+ T cell, CD8+ T cell, and NK cell counts were gradually decreased with the increased delayed hospitalization (p = 0.003, 0.002, 0.013, and 0.012; respectively). The proportion of T cell was gradually decreased but B cell was gradually increased with the increased delayed hospitalization (p = 0.031 and 0.003, respectively).Conclusion: T cell and CD4+ T cell counts negatively correlated with disease severity, CT manifestation and delayed hospitalization. CD4+ T cell was mainstay of immunity response in COVID-19 patients.

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Signals of Th2 immune response from COVID-19 patients requiring intensive care

Cited by 127 publications

References 5 publications

Alveolar Neutrophilic Recruitment in COVID-19 May Not be Mediated by Th17 Response

Alveolar Neutrophilic Recruitment in COVID-19 May Not be Mediated by Th17 Response

Lymphocyte subset alterations with disease severity, imaging manifestation, and delayed hospitalization in COVID-19 patients

Lymphocyte subset alterations with disease severity, imaging manifestation, and delayed hospitalization in COVID-19 patients

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