Bye Bye Bacterial Clearance

rather than a systemic suppression of immune responses or neutrophil function, influenza infection ACTIVATES IFN-γR SIGNALING and abrogates AM-DEPENDENT BACTERIA CLEARANCE and thereby causes EXTREME SUSCEPTIBILITY to pneumococcal infection.>
Importantly, using mice carrying conditional knockout
Ifngr1 gene in different myeloid cell subsets, we
demonstrate: influenza-induced IFN-γR signaling in AMs
IMPAIRS THEIR ANTIBACTERIAL FUNCTION, thereby
enabling otherwise noninvasive S. pneumoniae to cause
deadly pneumonia>
Influenza enables noninvasive Streptococcus pneumoniae to cause deadly pneumonia.
Influenza mainly predisposes hosts to airway, but not systemic, bacterial infection.
Influenza temporally abolishes innate bacterial clearance by alveolar macrophages
-Notably, in contrast to>
100% mortality in WT mice, ALL IFN-γR knockout (Ifngr1−/−) SURVIVED PR8/Spn coinfection...
-These results establish that rather than regulation of neutrophil function, MONONUCLEAR PHAGOCYTES are RESPONSIVE to the INHIBITORY EFFECT of IFN-γ on airway antibacterial defense.
Importantly, a selective deletion of Ifngr1 gene in CD11c+ cells (Cd11cCreIfngr1fl/fl, referred to as Ifngr1ΔAM/DC), mainly CD11c+Siglec-F+ AMs in the airway, resulted in significantly improved bacterial clearance after PR8/Spn coinfection...although DISPENSABLE FOR AIRWAY>
BACTERIAL CONTROL, NEUTROPHILS are essential for innate defense against systemic Spn infection.
...results suggests neutrophil-dependent systemic antibacterial defense is relatively competent after influenza infection. Importantly, the distinct outcomes of local versus systemic>
Spn superinfection suggest that, RATHER than DIRECTLY DISRUPTING EPITHELIAL BARRIER to promote systemic dissemination, influenza infection IMPAIRS AIRWAY ANTIBACTERIAL IMMUNITY to enable otherwise noninvasive S. pneumoniae to cause lethal pneumonia...we found that this influenza-
induced extreme susceptibility is attributable to IFN-γ signaling and abrogation of AM antibacterial function. Furthermore, by comparative analyses of mice with selective deletion of Ifngr1 gene in myeloid cells, AMs/DCs, macrophages/monocytes, or neutrophils...
influenza-induced IFN-γ signaling in AMs DIRECTLY IMPAIRS THEIR CAPABILITY FOR BACTERIAL CONTROL, thereby resulting in lethal bacterial outgrowth during secondary pneumococcal infection.
#IfYouCanControlYourBacteriaYouCantExpect2ControlYourLife.
Respiratory virus infection was associated with pneumococcal colonization and INCREASED Nasopharyngeal Pneumococcal Density. Similar elevated nasopharyngeal colonization densities have been described in influenza virus–infected animal models. The mechanism of this interaction is>
thought to be due to VIRUS-INDUCED INCREASE IN BACTERIAL attachment sites on nasopharyngeal epithelial cells. In addition, the MUCOUS PRODUCED AS A RESULT OF THE VIRAL INFECTION PROMOTES BACTERIAL GROWTH. This viral-bacterial interaction has been observed in children with>
A dynamic mucin mRNA signature associates with COVID-19 disease presentation and severity
insight.jci.org/articles/view/…
SC2 infection INDUCES MUCIN OVEREXPRESSION further promoting disease.>
We identified a dynamic #BLOODMUCIN #mRNA #SIGNATURE that clearly segregates symptomatic COVID from non-COVID pts. based on expression of MUC1, MUC2, MUC4, MUC6, MUC13, MUC16 and MUC20; and that discriminates between mild and critical
COVID based on the expression of MUC16, MUC20 and MUC21. Differences in the transcriptional landscape of mucins in critical cases compared to mild cases even identify associations with COVID symptoms, respiratory support, organ failure, secondary infections and mortality. #Mucins

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More from @janieyaya

16 Sep
Spike Protein from Virus or Vaxx is a toxin in the body and can "wake up" other latent viruses and bacteria and cause them to show symptoms, like swollen testicles or inflammation of the skin
Read 10 tweets
16 Sep
🎣Catch All the Fish🎣

An ABC news fishing expedition...took a STARTLING TURN...after a reporter asked readers to share stories of loved ones who DIED of Covid AFTER REFUSING or delaying to get the 💉.
INSTEAD, thousands reported of loved ones who died after💉.>
By noon on Monday, the post had RECEIVED over 39,000 angry and often heartbreaking RESPONSES. Virtually every string contains a FIRSTHAND report by people whose family members are GRIEVING THE LOSS OF LOVED ONES of all ages>
Reports of heart attacks and strokes abound: Image
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16 Sep
Government Geezers and FatCats are Superspreaders

we found that exhaled aerosol particles vary between subjects by 3 ORDERS OF MAGNITUDE, with exhaled respiratory droplet number increasing with degree of COVID infection and elevated BMI-years.>
We observed that 18% of SUBJECTS accounted for 80% of the EXHALED BIOAEROSOL.
The STRONG CORRELATION observed here between advanced BMI-years and GREATER PROPENSITY to GENERATE RESPIRATORY DROPLETS may be significant in the light of the recognized risk of those>
with high BMI, advanced age, or both (THE ELDERLY, the obese, and the OBESE ELDERLY) developing
severe symptoms upon COVID infection. Promiscuity of respiratory droplets in the airways heightens the probability that upper airway infection transports deeper into lungs, promoting>
Read 7 tweets
16 Sep
Go Where U Wanna Go

It doesn't stay in the muscle, circulates for several days, and is toxic to blood cells and endothelium of major organs.
Read 10 tweets
16 Sep
We know the answer. You are mandating a #WarpedSpeed 💉that is giving 20/30% Pts #LongCovid
See #IncellDx finding the S1 subunit in the blood of #PostVaxxLongCovid Pts.
Now you are doing it with @RedCross donations from #TheVaxxed. Think of the toxicity in vaxxed recipients.
Read 8 tweets

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