SUMMARYSevere Acute Respiratory Syndrome Coronavirus (SARS-CoV)-2 infection induces an exacerbated inflammation driven by innate immunity components. Dendritic cells (DCs) play a key role in the defense against viral infections, for instance plasmacytoid DCs (pDCs), have the capacity to produce vast amounts of interferon-alpha (IFN-α). In COVID-19 there is a deficit in DC numbers and IFN-α production, which has been associated with disease severity. In this work, we described that in addition to the DC deficiency, several DC activation and homing markers were altered in acute COVID-19 patients, which were associated with multiple inflammatory markers. Remarkably, previously hospitalized and non-hospitalized patients remained with decreased numbers of CD1c+ myeloid DCs and pDCs seven months after SARS-CoV-2 infection. Moreover, the expression of DC markers as CD86 and CD4 were only restored in previously non-hospitalized patients while integrin β7 and indoleamine 2,3- dyoxigenase (IDO) no restoration was observed. These findings contribute to a better understanding of the immunological sequelae of COVID-19.

Interleukin (IL)-8 concentrations were analyzed in 70 cerebrospinal fluid (CSF) samples from patients with meningitis of different etiologies and in 34 normal CSF samples. Patient groups included those with pyogenic meningitis, viral meningitis, self-resolving aseptic meningitis without a specific diagnosis, and meningitis of other etiologies and normal CSF from patients with and without neurologic disease. All samples from patients with pyogenic meningitis (18) but only 3 from patients with meningitis of other etiologies and with CSF polymorphonuclear leukocyte (PMNL) counts > or = 80% had IL-8 levels > or = 2.5 ng/mL. IL-8 was above the normal level (< or = 0.5 ng/mL) in samples from 5 of 13 viral and 8 of 23 self-resolving aseptic meningitis patients and in 7 of 13 samples from patients with meningitis caused by other microorganisms. There was a significant relationship between IL-8 levels and CSF PMNL counts in patients with nonpyogenic meningitis. The data suggest a possible role of IL-8 as PMNL chemotactic factor in different infections of the subarachnoid space, not only in pyogenic meningitis.

We assayed tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) concentrations in CSF from patients with meningitis of different etiologies and tested the usefulness of these assays for differentiating between pyogenic meningitis and aseptic meningitis of different etiologies. We used a monoclonal-antibody ELISA to test 125 CSF specimens from patients whose cases were classified as follows: pyogenic meningitis (n = 20), viral meningitis (n = 22), self-resolving aseptic meningitis for which no specific diagnosis was made (n = 25), meningitis due to other infectious agents (n = 11), and neoplastic meningitis (n = 5); we also tested normal CSF from healthy patients (n = 20) and those with neurological diseases (n = 22). Levels of TNF-alpha were above 200 pg/mL in 16 of 20 patients with pyogenic meningitis, but not in patients in the other groups. Levels of IL-1 beta were above 100 pg/mL in 15 of 20 patients with pyogenic meningitis and in one patient with a brain abscess. A positive correlation between levels of these cytokines and different inflammatory parameters was noted, whereas an inverse relationship with the duration of symptoms was observed. With regard to diagnosis, measurement of TNF-alpha and IL-1 beta levels showed sensitivities of 84.2% and 78.9%, respectively; specificities of 100% and 99%, respectively; a positive predictive value of 1 and 0.93, respectively; and a negative predictive value of 0.97 and 0.96, respectively.