Facilitated Expansion of Pneumococcal Colonization from the Nose to the Lower Respiratory Tract in Mice Preinfected with Influenza Virus

Takase, Hiroyuki; Nitanai, Hironobu; Yamamura, Eiko; Otani, Tomoyuki

doi:10.1111/j.1348-0421.1999.tb01226.x

Cited by 17 publications

(10 citation statements)

References 13 publications

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“…We found that susceptibility to S. pneumoniae was the greatest at 6 days after influenza infection and was not increased at 3 days after influenza infection. Several other groups have found similar results, and clinical evidence supports this timeframe for maximum susceptibility (14,24,42,59). Influenza-induced tissue damage is greatest after 6 days of influenza infection (44), and Plotkowski et al found that adherence of S. pneumoniae to influenza-infected tracheas was greatest after 6 days of influenza infection (48).…”

Section: Discussionsupporting

confidence: 65%

“…Previous studies have found that susceptibility to S. pneumoniae infection is greatest at 6 to 7 days after influenza infection (14,24,42,59). To validate our coinfection model, S. pneumoniae was inoculated into noninfected mice or mice infected with influenza for 3 or 6 days, and S. pneumoniae growth over 12 and 24 h was measured to determine when susceptibility to S. pneumoniae infection was greatest.…”

Section: Resultsmentioning

confidence: 99%

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Both Influenza-Induced Neutrophil Dysfunction and Neutrophil-Independent Mechanisms Contribute to Increased Susceptibility to a SecondaryStreptococcus pneumoniaeInfection

2006

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Since secondary Streptococcus pneumoniae infections greatly increase the mortality of influenza infections, we determined the relative roles of neutrophil-dependent and -independent mechanisms in increased susceptibility to S. pneumoniae during influenza infection. Mice infected with influenza for 6 days, but not 3 days, showed a significant increase in susceptibility to S. pneumoniae infection compared to mice not infected with influenza. There was significant neutrophil accumulation in the lungs of S. pneumoniae-infected mice regardless of whether or not they were infected with influenza for 3 or 6 days. Depletion of neutrophils in these mice resulted in increased susceptibility to S. pneumoniae in both the non-influenza-infected mice and mice infected with influenza for 3 days but not in the mice infected with influenza for 6 days, indicating that a prior influenza infection of 6 days may compromise neutrophil function, resulting in increased susceptibility to a S. pneumoniae infection. Neutrophils from the lungs of mice infected with influenza for 3 or 6 days exhibited functional impairment in the form of decreased phagocytosis and intracellular reactive oxygen species generation in response to S. pneumoniae. In addition, neutrophil-depleted mice infected with influenza for 6 days were more susceptible to S. pneumoniae than neutrophil-depleted mice not infected with influenza, indicating that neutrophil-independent mechanisms also contribute to influenza-induced increased susceptibility to S. pneumoniae. Pulmonary interleukin-10 levels were increased in coinfected mice infected with influenza for 6 days but not 3 days. Thus, an influenza infection of 6 days increases susceptibility to S. pneumoniae by both suppression of neutrophil function and by neutrophil-independent mechanisms such as enhanced cytokine production.

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Section: Discussionsupporting

confidence: 65%

Section: Resultsmentioning

confidence: 99%

Both Influenza-Induced Neutrophil Dysfunction and Neutrophil-Independent Mechanisms Contribute to Increased Susceptibility to a SecondaryStreptococcus pneumoniaeInfection

2006

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“…Co-infection of influenza A with S. pneumoniae resulted in severe morbidity with a 75% death rate within 40 h, clear evidence of the consequences of co/secondary bacterial infection (Berendt et al, 1975). These findings are reflected in several other studies, with some even showing that co-infection may assist in the spreading of S. pneumoniae infection to the lower respiratory tract (Takase et al, 1999; Seki et al, 2004). …”

Section: Pathobionts Associated With Co/secondary Bacterial Infectionsupporting

confidence: 59%

Secondary Bacterial Infections Associated with Influenza Pandemics

2017

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Lower and upper respiratory infections are the fourth highest cause of global mortality (Lozano et al., 2012). Epidemic and pandemic outbreaks of respiratory infection are a major medical concern, often causing considerable disease and a high death toll, typically over a relatively short period of time. Influenza is a major cause of epidemic and pandemic infection. Bacterial co/secondary infection further increases morbidity and mortality of influenza infection, with Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus reported as the most common causes. With increased antibiotic resistance and vaccine evasion it is important to monitor the epidemiology of pathogens in circulation to inform clinical treatment and development, particularly in the setting of an influenza epidemic/pandemic.

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“…The trachea is thought to play a role in the progression of S. pneumoniae from the nasal mucosa, where it asymptomatically colonizes the nasal epithelium, to the lungs, resulting in pneumonia (15,44). Changes to the tracheal epithelium induced by influenza virus may increase susceptibility to a secondary S. pneumoniae infection by increasing pneumococcal adherence to the tracheal epithelium and/or decreasing the clearance of S. pneumoniae via the mucociliary escalator of the trachea, because many of the ciliated cells are destroyed (15,24).…”

Section: Discussionmentioning

confidence: 99%

Influenza Virus Infection Decreases Tracheal Mucociliary Velocity and Clearance ofStreptococcus pneumoniae

Pittet

Hall-Stoodley²,

Rutkowski³

et al. 2010

Am J Respir Cell Mol Biol

190

147

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Influenza virus infections increase susceptibility to secondary bacterial infections, such as pneumococcal pneumonia, resulting in increased morbidity and mortality. Influenza-induced tissue damage is hypothesized to increase susceptibility to Streptococcus pneumoniae infection by increasing adherence to the respiratory epithelium. Using a mouse model of influenza infection followed by S. pneumoniae infection, we found that an influenza infection does not increase the number of pneumococci initially present within the trachea, but does inhibit pneumococcal clearance by 2 hours after infection. To determine whether influenza damage increases pneumococcal adherence, we developed a novel murine tracheal explant system to determine influenza-induced tissue damage and subsequent pneumococcal adherence. Murine tracheas were kept viable ex vivo as shown by microscopic examination of ciliary beating and cellular morphology using continuous media flow for up to 8 days. Tracheas were infected with influenza virus for 0.5-5 days ex vivo, and influenza-induced tissue damage and the early stages of repair to the epithelium were assessed histologically. A prior influenza infection did not increase pneumococcal adherence, even when the basement membrane was maximally denuded or during the repopulation of the basement membrane with undifferentiated epithelial cells. We measured mucociliary clearance in vivo and found it was decreased in influenza-infected mice. Together, our results indicate that exposure of the tracheal basement membrane contributes minimally to pneumococcal adherence. Instead, an influenza infection results in decreased tracheal mucociliary velocity and initial clearance of pneumococci, leading to an increased pneumococcal burden as early as 2 hours after pneumococcal infection.

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Facilitated Expansion of Pneumococcal Colonization from the Nose to the Lower Respiratory Tract in Mice Preinfected with Influenza Virus

Cited by 17 publications

References 13 publications

Both Influenza-Induced Neutrophil Dysfunction and Neutrophil-Independent Mechanisms Contribute to Increased Susceptibility to a SecondaryStreptococcus pneumoniaeInfection

Both Influenza-Induced Neutrophil Dysfunction and Neutrophil-Independent Mechanisms Contribute to Increased Susceptibility to a SecondaryStreptococcus pneumoniaeInfection

Secondary Bacterial Infections Associated with Influenza Pandemics

Influenza Virus Infection Decreases Tracheal Mucociliary Velocity and Clearance ofStreptococcus pneumoniae

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