Editorial: Global excellence in inflammatory diseases: North America 2021

COPYRIGHT © 2023 Kusner, Misra and Lucas. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. TYPE Editorial PUBLISHED 06 July 2023 DOI 10.3389/fimmu.2023.1245827

The majority of manuscripts briefly discuss emerging therapeutic approaches aimed at mitigating inflammatory diseases, along with the associated challenges.
Orecchioni et al. elaborate in their concise review on their recent findings that olfactory receptors (ORs), which bind odorous ligands, are not only expressed in the nasal olfactory epithelium, but also in extranasal macrophages. The review discusses how activation of different ORs in macrophages with either octanol on the one hand or with lactate on the other hand can aggravate inflammasome activation in atherosclerosis or dampen the immune response in cancer, respectively. In view of these landmark findings, the authors advocate the need for deorphanizing more ORs and determining the sources of their ligands, which can foster the development of novel anti-inflammatory therapies.
Padgett et al. contribute with an original study aiming to investigate how the little known non-classical CD16 + monocytes influence the CD8 + effector T cell-mediated anti-tumor response in mice injected with the B16F10-OVA melanoma cell line. To do so, the authors compare tumor progression between wild type mice and an in-house developed E2 -/mouse strain, which specifically lacks non-classical monocytes following depletion of the Nr4a1 E2 super enhancer subdomain, while preserving classical monocyte frequencies and macrophage function.
Paudel et al. provide a comprehensive review of the emerging concepts the hematopoietic system uses during acute inflammatory diseases (e.g. pneumonia and sepsis) to rapidly switch from steady state to emergency granulopoiesis. This switch is necessary to augment neutrophil production in the bone marrow and to release them to the blood, from where they are recruited in large numbers to peripheral organs to cope with demand. However, when recruited in excessive numbers, neutrophils can induce severe organ injury (like in the lungs). The review also reassesses the well-established cellular and molecular mechanisms associated with granulopoiesis and as such fosters the reader's understanding of the mechanisms governing granulopoiesis, which is critical to modulate the detrimental inflammatory process in numerous organs following infectious assault.
Thanks to anti-retroviral therapy, HIV patients have a comparable life span to non-infected subjects, but they unfortunately have a higher tendency to develop life-threatening pulmonary hypertension (PH), due to the chronic inflammation in their lungs. Currently, small animal models combining HIV infection with PH do not accurately represent the human condition. Rodriguez-Irizarry et al. combine HIV infection with the PH-inducing VEGF antagonist SU5416 in humanized NSG mice. The main aim is to evaluate whether this represents a valid translational small animal model for PH in HIV patients. The second aim of their studies is to detect inflammatory mediators that are increased upon combining both insults, with a focus on endothelialmonocyte activating polypeptide II (EMAP II).
Unilateral ureteral obstruction (UUO) injury in mice represents a translational model of Interstitial Fibrosis and Tubular Atrophy (IFTA), the most common cause of long-term graft failure following renal transplant, characterized by interstitial fibrosis and the loss of Myasthenia Gravis (MG) is a neuromuscular autoimmune disorder characterized by chronic fatigue of the eye muscles as well as other skeletal muscles. The muscle weakness occurs primarily as a consequence of the binding of an autoantibody to the acetylcholine receptors, which abrogates normal neuromuscular signal transmission. Huda provides an update on the association and correlation of inflammation with the initiation, progression and severity of MG. The concise review focuses on immune cell interactions (MF, T H , T regs , T H 17, B cells, DC) the role of immunomodulator molecules in disease development (pro-inflammatory cytokines and chemokines) and critically discusses current therapeutic strategies targeting inflammation in MG (including combination therapy targeting both components, auto-antibody and inflammation).
The use of nicotine-containing e-cigarettes has rapidly increased in recent years. Aerosols produced through the use of e-cigarettes can be immunosuppressive and pro-inflammatory. Influenza A virus infection (IAV) is one of the main causes of viral pneumonia, accompanied by intense inflammation. IAV-induced pneumonia can cause potentially lethal acute respiratory distress syndrome and a good host response to infection is crucial. Maishan et al. provide results from an original study investigating and comparing the effects of, on the one hand aerosolized e-cigarette carrier [vegetable glycerin (VG) and propylene glycol (PG)] and on the other hand aerosolized carrier (VG/PG) with nicotine, on i) the pro-inflammatory response to IAV-induced pneumonia, ii) the transcriptomic response to the pathogen, iii) host defense mechanisms, iv) lung barrier integrity and v) viral clearance during IAV infection. They moreover focus on the presence of Mucin 5 subtype AC (MUC5AC) in the distal airspaces, a compound shown to be protective and to improve viral clearance in IAV infection.
This Research Topic only addresses a selection of the vast subject of inflammatory diseases. For more updates on these and other inflammatory diseases, the authors refer the reader to other recent Research Topic on this topic in Frontiers in Immunology -Inflammation, such as "Advances in Autoimmune Myasthenia Gravis" (1), "Autoimmunity and Chronic Inflammation in Early Life" (2) and "Insights in Inflammation 2022" (3).

Author contributions
RL wrote the original manuscript. LK and RM edited and approved the manuscript.

Funding
LK received a pilot award through the Myasthenia Gravis Foundation of America, NIH funding from grant 5U54NS115054, as well as industry funding from MimiVax LLC, Amplo Biotechnology, Alnylam Pharmaceuticals and CSL Behring. RM received funding from NIH/NHLBI grants 5U01HL148861 and 1U54HL165443. RL was funded by a TPA award from the American Heart Association 23TPA1072536 and by NIH/NHLBI grant R01 HL138410, as well as Bridge funding from the office of the Senior Vice President for Research at Augusta University. The industry funders listed for LK were not involved in the writing of this editorial or the decision to submit it for publication.