scholarly journals Resident memory CD8+T cells in the upper respiratory tract prevent pulmonary influenza virus infection

2017 ◽  
Vol 2 (12) ◽  
pp. eaam6970 ◽  
Author(s):  
Angela Pizzolla ◽  
Thi H. O. Nguyen ◽  
Jeffrey M. Smith ◽  
Andrew G. Brooks ◽  
Katherine Kedzierska ◽  
...  
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Virus Infection ◽  
Respiratory Tract ◽  
Cd8 T Cells ◽  
Influenza Virus Infection ◽  
Upper Respiratory Tract ◽  
Memory Cd8 T Cells ◽  
Upper Respiratory

scholarly journals Effect of Intranasal Administration ofLactobacillus casei Shirota on Influenza Virus Infection of Upper Respiratory Tract in Mice

2001 ◽  
Vol 8 (3) ◽  
pp. 593-597 ◽  
Author(s):  
Tetsuji Hori ◽  
Junko Kiyoshima ◽  
Kan Shida ◽  
Hisako Yasui
Keyword(s):  
Influenza Virus ◽  
Survival Rate ◽  
Virus Infection ◽  
Respiratory Tract ◽  
Intranasal Administration ◽  
Control Level ◽  
Influenza Virus Infection ◽  
Control Group ◽  
Upper Respiratory Tract ◽  
Upper Respiratory

ABSTRACT In mice administered Lactobacillus casei strain Shirota (LcS) intranasally, potent induction of interleukin 12, gamma interferon, and tumor necrosis factor alpha, which play a very important role in excluding influenza virus (IFV), was evident in mediastinal lymph node cells. In this model of upper respiratory IFV infection, the titers of virus in the nasal wash of mice inoculated with 200 μg of LcS for three consecutive days (LcS 200 group) before infection were significantly (P < 0.01) lower than those of mice not inoculated with LcS (control group) (100.9 ± 0.6 versus 102.1 ± 1.0). The IFV titer was decreased to about 1/10 of the control level. Using this infection model with modifications, we investigated whether the survival rate of mice was increased by intranasal administration of LcS. The survival rate of the mice in the LcS 200 group was significantly (P < 0.05) greater than that of the mice in the control group (69% versus 15%). It seems that the decrease in the titer of virus in the upper respiratory tract to 1/10 of the control level was important in preventing death. These findings suggest that intranasal administration of LcS enhances cellular immunity in the respiratory tract and protects against influenza virus infection.

scholarly journals Osteopontin Modulates the Generation of Memory CD8+T Cells during Influenza Virus Infection

2011 ◽  
Vol 187 (11) ◽  
pp. 5671-5683 ◽  
Author(s):  
Junko Morimoto ◽  
Kayoko Sato ◽  
Yosuke Nakayama ◽  
Chiemi Kimura ◽  
Kiichi Kajino ◽  
...  
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Virus Infection ◽  
Cd8 T Cells ◽  
Influenza Virus Infection ◽  
Memory Cd8 T Cells

scholarly journals In situ imaging reveals different responses by naïve and memory CD8 T cells to late antigen presentation by lymph node DC after influenza virus infection

2008 ◽  
Vol 38 (12) ◽  
pp. 3304-3315 ◽  
Author(s):  
Kamal M. Khanna ◽  
Carolina C. Aguila ◽  
Jason M. Redman ◽  
Jenny E. Suarez-Ramirez ◽  
Leo Lefrançois ◽  
...  
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Lymph Node ◽  
Virus Infection ◽  
Antigen Presentation ◽  
Cd8 T Cells ◽  
Influenza Virus Infection ◽  
Memory Cd8 T Cells ◽  
Late Antigen

scholarly journals Nasal-associated lymphoid tissues (NALTs) support the recall but not priming of influenza virus-specific cytotoxic T cells

2017 ◽  
Vol 114 (20) ◽  
pp. 5225-5230 ◽  
Author(s):  
Angela Pizzolla ◽  
Zhongfang Wang ◽  
Joanna R. Groom ◽  
Katherine Kedzierska ◽  
Andrew G. Brooks ◽  
...  
Keyword(s):  
T Cells ◽  
Influenza Virus ◽  
Respiratory Tract ◽  
Lymphoid Tissue ◽  
Cytotoxic T Lymphocyte ◽  
Influenza Virus Infection ◽  
Nasal Passage ◽  
Lymphoid Tissues ◽  
Upper Respiratory Tract ◽  
Upper Respiratory

The lymphoid tissue that drains the upper respiratory tract represents an important induction site for cytotoxic T lymphocyte (CTL) immunity to airborne pathogens and intranasal vaccines. Here, we investigated the role of the nasal-associated lymphoid tissues (NALTs), which are mucosal-associated lymphoid organs embedded in the submucosa of the nasal passage, in the initial priming and recall expansion of CD8+ T cells following an upper respiratory tract infection with a pathogenic influenza virus and immunization with a live attenuated influenza virus vaccine. Whereas NALTs served as the induction site for the recall expansion of memory CD8+ T cells following influenza virus infection or vaccination, they failed to support activation of naïve CD8+ T cells. Strikingly, NALTs, unlike other lymphoid tissues, were not routinely surveyed during the steady state by circulating T cells. The selective recruitment of memory T cells into these lymphoid structures occurred in response to infection-induced elevation of the chemokine CXCL10, which attracted CXCR3+ memory CD8+ T cells. These results have significant implications for intranasal vaccines, which deliver antigen to mucosal-associated lymphoid tissue and aim to elicit protective CTL-mediated immunity.

scholarly journals Salivary Blockade Protects the Lower Respiratory Tract of Mice from Lethal Influenza Virus Infection

2017 ◽  
Vol 91 (14) ◽  
Author(s):  
Karen Ivinson ◽  
Georgia Deliyannis ◽  
Leanne McNabb ◽  
Lara Grollo ◽  
Brad Gilbertson ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Respiratory Tract ◽  
Lower Respiratory Tract ◽  
Influenza A ◽  
Lethal Dose ◽  
Laboratory Mouse ◽  
Influenza Virus Infection ◽  
Upper Respiratory Tract ◽  
Upper Respiratory

ABSTRACT It is possible to model the progression of influenza virus from the upper respiratory tract to the lower respiratory tract in the mouse using viral inoculum delivered in a restricted manner to the nose. In this model, infection with the A/Udorn/307/72 (Udorn) strain of virus results ultimately in high viral titers in both the trachea and lungs. In contrast, the A/Puerto Rico/8/34 (PR8) strain causes an infection that is almost entirely limited to the nasal passages. The factors that govern the progression of virus down the respiratory tract are not well understood. Here, we show that, while PR8 virus grows to high titers in the nose, an inhibitor present in the saliva blocks further progression of infection to the trachea and lungs and renders an otherwise lethal dose of virus completely asymptomatic. In vitro, the salivary inhibitor was capable of potent neutralization of PR8 virus and an additional 20 strains of type A virus and two type B strains that were tested. The exceptions were Udorn virus and the closely related H3N2 strains A/Port Chalmers/1/73 and A/Victoria/3/75. Characterization of the salivary inhibitor showed it to be independent of sialic acid and other carbohydrates for its function. This and other biochemical properties, together with its virus strain specificity and in vivo function, indicate that the mouse salivary inhibitor is a previously undescribed innate inhibitory molecule that may have evolved to provide pulmonary protection of the species from fatal influenza virus infection. IMPORTANCE Influenza A virus occasionally jumps from aquatic birds, its natural host, into mammals to cause outbreaks of varying severity, including pandemics in humans. Despite the laboratory mouse being used as a model to study influenza virus pathogenesis, natural outbreaks of influenza have not been reported in the species. Here, we shed light on one mechanism that might allow mice to be protected from influenza in the wild. We show that virus deposited in the mouse upper respiratory tract will not progress to the lower respiratory tract due to the presence of a potent inhibitor of the virus in saliva. Containing inhibitor-sensitive virus to the upper respiratory tract renders an otherwise lethal infection subclinical. This knowledge sheds light on how natural inhibitors may have evolved to improve survival in this species.

scholarly journals Respiratory Commensal Bacteria Reduce the Immune Damage Caused by Influenza Virus Infection by Regulating the Polarization State of Alveolar Macrophages

2021 ◽  
Author(s):  
Liang Chen ◽  
Limei Zhu ◽  
Ying Qi
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Virus Infection ◽  
Respiratory Tract ◽  
Alveolar Macrophages ◽  
Influenza Virus Infection ◽  
Commensal Bacteria ◽  
Bioactive Molecules ◽  
Inflammatory Factors ◽  
Upper Respiratory Tract

Abstract BackgroundThe Role of respiratory tract commensal bacteria in maintaining the immune homeostasis of the respiratory tract is not well eluciated. We aimed to analyze the effect of respiratory symbiotic bacteria on respiratory immune system and its immune response to exogenous pathogens.MethodsIn this study, SPF C57BL/6 male mice were sensitized by nasal drip of respiratory tract symbiotic bacteria s. aurcus for 6-8 weeks and then used to establish a s. aureus upper respiratory tract symbiosis mouse model. Subsequently, the mice were infected with influenza virus through nasal drip to establish a virus infection model. During the experiment, the immunopathological damage, cytokines and mechanisms related to immune response were analyzed and studied.ResultsThe study found that in the s.aureus upper respiratory tract symbiosis mouse model, s.aurcus sensitization significantly reduced the immune damage in the lungs caused by influenza virus A (IVA) infection, but this protective effect was significantly weakened when alveolar macrophages were cleared. Further studies found that during influenza virus infection, M2 alveolar macrophages (AM) secreted regulatory cytokines to suppress the excessive immune response induced by influenza virus infection. α7nAChR agonist GTS-21 could reduce inflammation in lung tissues, the amount of AM and the expression of inflammatory factors, and the secretion and expression of high-mobility group box 1 (HMGB1) in lung tissues, plasma and bronchoalveolar lavage fluid (BALF). GTS-21 also reduced the lung injury caused by IVA in mice and the levels of M1 type AM bioactive molecules inducible NO synthase (iNOS) and pro-inflammatory factors in AM, and increased the levels of M2 type AM bioactive molecules Arg1 and Ym1. Anti-HMGB 1 antibody reduced the inflammation of lung tissues of mice caused by IVA and inhibited the polarization of AM to M1. Recombinant HMGB1 (rHMGB1) increased the inflammation of lung tissues of mice caused by IVA and promoted the polarization of AM to M1.ConclusionsRespiratory commensal bacteria induced M2 alveolar macrophages with immunomodulatory function to protect the host against illness and death caused by IVA infection.

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