Professor Cossarizza began his talk by highlighting the major role inflammation (and hyper inflammation) play in COVID-19 pathogenesis. He also briefly described inflammatory immune responses that occur in the lung during the late stages of COVID-19 and how immune cell functions aimed at reducing SARS-CoV-2 burden can contribute to further inflammation and have detrimental effects (host cell damage).
Pregnancy and ageing are associated with skewing of immune responses towards pro-Th2 immune responses and inflammageing (pro-th1 inflammation), respectively. Using mass cytometry his research group characterised T and B cell phenotypes in pregnant women with o SARS-Cov-2 infection and (asymptomatic or paucisymptomatic) COVID-19. Interestingly, majority of immune responses between SARS-CoV-2 infected and uninfected pregnant women were not different with exception of higher frequencies of low-density neutrophils in COVID-19+ pregnant women. Analysis of serum cytokine and chemokine levels illustrated increased levels of inflammatory antagonists in COVD-19+ pregnant women compared to uninfected pregnant women (see figure). Additionally, none of the SARS-CoV-2 infected pregnant women experienced complications associated with infection, thus suggesting that if COVId-19 remains asymptomatic and mild, it may have no risk to pregnancy.
Characterisation of immune responses in aged individuals (<60 vs >70 years old) with COVID-19 illustrated lower levels of central memory CD4+ T, naïve CD8+ T and B cell memory cells, and higher levels of plasmablasts in > 70-year-olds compared with < 60-year-olds. Additionally, they observed differences in cytokine and chemokine levels between the two age groups which were characteristic of increased inflammation in > 70-year-olds compared with < 60-year-olds. Thus, suggesting that inflammaging likely potentiates COVID-19 associated inflammation resulting in further damage to tissues and organs.
