Author: Mx

When the new coronavirus (COVID-19) becomes severe, cytokine storms occur and develop acute respiratory distress syndrome (ARDS). For this treatment, from the viewpoint of immune control, il-6 inhibitors such as tocilizumab (actemula) and steroids that suppress inflammation are used.

The Yale School of Medicine group reports from randomized, placebo-controlled trials that systemic corticosteroids are more therapeutic and the effects of tocilizumab are not clear.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7781335/

As shown in the figure below, the behavior of covid-19 biomarkers is very different between corticosteroids and tocilizumab. Perhaps, it is because the effect is limited even if a single cytokine is inhibited.

A group of University College London has reported on the prognostic symptoms of the new coronavirus (COVID-19).
https://f1000research.com/articles/9-1349/v1

Ms analysis of 96 inflammatory and anti-inflammatory protein panels suggests that changes remain in inflammatory biomarkers and stress-induced biomarkers for more than 40 days after suffering from COVID-19.
Specifically, it is said that the effects of the following six biomarkers remain after the disease.

peroxiredoxin 3 (PRDX3)
carbamoyl phosphate synthase (CPS1)
N-Myc downstream regulated gene 1 (NDRG1)
Collagen triple helix repeat containing 1 (CTHRC1)
Cystatin C (CYTC)
Progranulin (GRN)

A group of The Memorial Hospital Group, Istanbul, Turkey groups has made an interesting report that urine foaming can be an effective indicator for diagnosing and predicting the prognosis of COVID-19.
http://www.nclin.ist/jvi.aspx?un=NCI-42027&volume=

The urine of patients hospitalized for COVID-19 or in ICU was reddish from orange in color, and the new coronavirus was diagnosed by collecting urine with a test tube and observing the foaming condition after shaking for 15 seconds.
The accuracy of the diagnosis was 92% sensitivity and 89% specificity.

The urine of healthy people is usually light yellow to light yellow-brown, and there is no basic problem if urine bubbles disappear shortly after urination.
However, it is well known that the color of urine changes with the disease state, and
when urobilinogen, urine protein and urine sugar in the urine increase, it becomes more foamy.

It may be reasonable to think of it as a reference only.

A group of Univ. of Virginia Health System has reported interesting phenomena on the expression of IgG, IgA, and IgM in the new coronavirus (COVID-19).
https://www.medrxiv.org/content/10.1101/2020.12.05.20244541v1

IgG, IgM, and IgA are highly expressed as COVID-19 becomes severe.
IL-10 and IgG inversely correlate.

Cytokine IL-10 is usually thought to be an anti-inflammatory one.
IL-10 and IgG are inversely correlated, and moreover, IgG is highly expressed as the disease becomes severe,
Does this mean that IL-10 works as an inflammatory cytokine?

Lectins with ricin B chains are collectively referred to as R-type lectins.
Ricin is galactose-specific, but the ricin-like structure has an extremely wide biological distribution and has various specificities such as sialic acid, mannose, xylose, etc. in addition to galactose.
The R-type lectin "Sevil" from mussel Mytilisepta virgata binds particularly strongly to the asialo-GM1 structure.
From the Yokohama City University Group,
https://www.nature.com/articles/s41598-020-78926-7

Dendritic cells (DCs) are at the forefront of the immune reaction.
When pathogens such as viruses invade, Toll-like receptors (TLR) and C-type lectin receptors (CLRs) expressed on DCs recognize the molecular structure peculiar to pathogens and trigger immune responses.
The CLR of DCs includes DCIR/CD367/CLEC4A, DECTIN1/CD369/CLEC7A, DECTIN2/CLEC6A, DNGR1/CD370/CLEC9A, MMR/CD206, DEC205/CD205, DC-SIGN/CD209, langerin/CD207, BDCA2/CD303/CLEC4C, etc.
The function of these lectins remain largely unknow, but for example,
DCIR binds to high mannose/fucose glycans and works inhibitory on the secretion of IL12 and TNFα, while DECTIN1 recognizes β-1,3-glucans and conversely promotes the secretion of these inflammatory cytokines.

A group of Univ. Grenoble Alpes discussed how the expression of various CLRs changes in chronic HBV based on experimental results performed using Flow cytometry.
https://onlinelibrary.wiley.com/doi/10.1002/cti2.1208

There are three subclasses of DC: CD1c/BDCA1 (cDC2s), CD141/BDCA3 (cDC1s), and plasmacytoid DCs (pDCs).

Blood cDC2s: DECTIN1, MMR decreased,
Liver cDC2s: DCIR, MMR decreased,
Blood cDC1s: DECTIN1, CLEC9A decreased, Fcɣ Receptor increased slightly,
Liver cDC1s: DCIR, CLEC9A, Fcɣ receptor, MMR decreased, DECTIN1 increased slightly,
Blood pCDs: Little change,
Liver pCDs: DCIR increased, Fcε receptor increased slightly.

Such a change is happening.

Although the changes are very complex, it is worth noting that chronic HBV causes changes in the expression of CLRs in DCs.
Overall, CLR expression seems to be decreasing, which makes it easier for HBV to escape from immune system, right?

A group of AIST and Kyoto Univ. has discovered a high-performance novel exosome marker as a novel marker for Alzheimer's disease.
https://pubmed.ncbi.nlm.nih.gov/33345458/

They found that in patients with Alzheimer's disease, there was a significant difference in glycan modification of exosomes compared to healthy people, and the exosomes were highly high mannosylated.
Using a high mannose specific lectin, its lectin blotting revealed a very strong band around 80 kDa, which was identified as a marker of exosomes, CD61.

A sandwich assay (Tim4-αCD63) assembled with an antibody to the exosome marker CD63 and Tim4 (T cell immunoglobulin and mucin domain-containing protein 4) showed the highest discriminating ability among (CD61, CD41, CD63, and CD9), and the obtained AUC reached 0.957.