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Antimicrobial Peptides, Cytokines, Chemokines and Danger Molecules in Immunity and Autoimmunity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 30 April 2024 | Viewed by 1280

Special Issue Editor

Special Issue Information

Dear Colleagues,

Antimicrobial peptides and antimicrobial chemokines can act both as protein mediators of specific immunological and non-immunological pathways or as chemo-attractants for immune cells. It is the case of cathelicidin LL37, which has chemo-extractant roles for immune cells and also acts as a “danger signal” and stimulator of the immune response, when bound to nucleic acids, with important effects in immunity and autoimmunity. A similar role is played by CXCL4, also called platelet factor 4 (PF4), which is a chemokine with pleiotropic effector functions but also a trigger of TLR-mediated inflammation in complexes with DNA/RNA. Both LL37 and CXCL4 play a role in immunity and autoimmunity. Other cationic molecules, either produced endogenously in humans or of microbial origin, can have TLR triggering capacity if bound to nucleic acids. Interestingly, these kinds of mediators can also be post-translationally modified during inflammation. In this Research Topic, we invite original articles and reviews illustrating current research and opinions about molecules that have pleiotropic effects on immunity and the effect of their post-translational modifications on health and disease. The topic involves but is not limited to, DNA/RNA binding proteins that exert pro-inflammatory role in immunity and autoimmunity and the effect of post-translational modification on their functions during normal immune responses and in immune-mediated diseases.

Dr. Loredana Frasca
Guest Editor

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Keywords

  • antimicrobial peptides
  • antimicrobial chemokines
  • immune cells
  • immune responses
  • autoimmunity

Published Papers (2 papers)

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Research

13 pages, 2796 KiB  
Article
Genital Dysbiosis and Different Systemic Immune Responses Based on the Trimester of Pregnancy in SARS-CoV-2 Infection
by Giuseppina Campisciano, Alice Sorz, Carolina Cason, Nunzia Zanotta, Fabrizia Gionechetti, Maria Piazza, Petra Carli, Francesca Maria Uliana, Lisa Ballaminut, Giuseppe Ricci, Francesco De Seta, Gianpaolo Maso and Manola Comar
Int. J. Mol. Sci. 2024, 25(8), 4298; https://doi.org/10.3390/ijms25084298 - 12 Apr 2024
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Abstract
Respiratory infections are common in pregnancy with conflicting evidence supporting their association with neonatal congenital anomalies, especially during the first trimester. We profiled cytokine and chemokine systemic responses in 242 pregnant women and their newborns after SARS-CoV-2 infection, acquired in different trimesters. Also, [...] Read more.
Respiratory infections are common in pregnancy with conflicting evidence supporting their association with neonatal congenital anomalies, especially during the first trimester. We profiled cytokine and chemokine systemic responses in 242 pregnant women and their newborns after SARS-CoV-2 infection, acquired in different trimesters. Also, we tested transplacental IgG passage and maternal vaginal–rectal microbiomes. IgG transplacental passage was evident, especially with infection acquired in the first trimester. G-CSF concentration—involved in immune cell recruitment—decreased in infected women compared to uninfected ones: a beneficial event for the reduction of inflammation but detrimental to ability to fight infections at birth. The later the infection was acquired, the higher the systemic concentration of IL-8, IP-10, and MCP-1, associated with COVID-19 disease severity. All infected women showed dysbiosis of vaginal and rectal microbiomes, compared to uninfected ones. Two newborns tested positive for SARS-CoV-2 within the first 48 h of life. Notably, their mothers had acute infection at delivery. Although respiratory infections in pregnancy are reported to affect babies’ health, with SARS-CoV-2 acquired early during gestation this risk seems low because of the maternal immune response. The observed vaginal and rectal dysbiosis could be relevant for neonatal microbiome establishment, although in our series immediate neonatal outcomes were reassuring. Full article
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23 pages, 5112 KiB  
Article
ERK1/2-CEBPB Axis-Regulated hBD1 Enhances Anti-Tuberculosis Capacity in Alveolar Type II Epithelial Cells
by Yaoxin Chen, Zhenyu Han, Sian Zhang, Honglin Liu, Ke Wang, Jieyu Liu, Feichang Liu, Shiyun Yu, Na Sai, Haiyan Mai, Xinying Zhou, Chaoying Zhou, Qian Wen and Li Ma
Int. J. Mol. Sci. 2024, 25(4), 2408; https://doi.org/10.3390/ijms25042408 - 18 Feb 2024
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Abstract
Tuberculosis, caused by Mycobacterium tuberculosis (Mtb), remains a global health crisis with substantial morbidity and mortality rates. Type II alveolar epithelial cells (AEC-II) play a critical role in the pulmonary immune response against Mtb infection by secreting effector molecules such as antimicrobial peptides [...] Read more.
Tuberculosis, caused by Mycobacterium tuberculosis (Mtb), remains a global health crisis with substantial morbidity and mortality rates. Type II alveolar epithelial cells (AEC-II) play a critical role in the pulmonary immune response against Mtb infection by secreting effector molecules such as antimicrobial peptides (AMPs). Here, human β-defensin 1 (hBD1), an important AMP produced by AEC-II, has been demonstrated to exert potent anti-tuberculosis activity. HBD1 overexpression effectively inhibited Mtb proliferation in AEC-II, while mice lacking hBD1 exhibited susceptibility to Mtb and increased lung tissue inflammation. Mechanistically, in A549 cells infected with Mtb, STAT1 negatively regulated hBD1 transcription, while CEBPB was the primary transcription factor upregulating hBD1 expression. Furthermore, we revealed that the ERK1/2 signaling pathway activated by Mtb infection led to CEBPB phosphorylation and nuclear translocation, which subsequently promoted hBD1 expression. Our findings suggest that the ERK1/2-CEBPB-hBD1 regulatory axis can be a potential therapeutic target for anti-tuberculosis therapy aimed at enhancing the immune response of AEC-II cells. Full article
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