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Comment
. 2023 Apr 15;207(8):1105-1107.
doi: 10.1164/rccm.202212-2314LE.

Novel Insight into Pulmonary Fibrosis and Long COVID

Jan C Kamp  1   2 , Christopher Werlein  3   2 , Edith K J Plucinski  3   2 , Lavinia Neubert  3   2 , Tobias Welte  1   2 , Peter D Lee  4 , Paul Tafforeau  5 , Claire Walsh  6 , Mark P Kuehnel  3   2 , Detlef Schuppan  7   8 , Marius M Hoeper  1   2 , Danny D Jonigk  2   9 , Maximilian Ackermann  10   11
Affiliations
Comment

Novel Insight into Pulmonary Fibrosis and Long COVID

Jan C Kamp et al. Am J Respir Crit Care Med. .
No abstract available

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Figures

Figure 1.
Figure 1.
(A) The trajectory of severe and fatal pulmonary coronavirus disease (COVID-19) is driven by a time-dependent evolution of different pathomechanisms. Initially, there is high inflammatory activity promoting microthrombosis with consecutive lobular microischemia and tissue hypoxia. This, in turn, leads to a rapid and aberrant expansion of the vascular plexus by progressive intussusceptive neoangiogenesis, which appears to drive fibrotic tissue remodeling and to contribute to the long-term physical impairment known as long COVID syndrome. This cascade-like pathophysiology is based on the sequential expression of distinct markers. (B) Venn diagram of selected differentially expressed genes compared with control samples (adjusted P ⩽ 0.05). Comparative analysis demonstrated an overlap between usual interstitial pneumonia (UIP), nonspecific interstitial pneumonia (NSIP), and COVID-19. (C) Histologic comparison of COVID-19 and different interstitial lung diseases (ILDs). (a) Early COVID-19 with diffuse alveolar damage showing hyaline membranes (indicated by an arrowhead). (b) Post-COVID chronic interstitial fibrosis in explanted lungs with an NSIP-like pattern. (c and d) Late COVID-19 (>7 days of hospitalization before death)–associated changes with rather unspecific interstitial thickening of alveolar septae (c) and organizing pneumonia (OP)-like changes (d, arrowhead). (e–h) These patterns were compared with different ILD patterns of (e) UIP with foci of activated fibroblasts (arrowhead), (f) NSIP with homogeneous thickened alveolar septae, (g) OP with intraalveolar mesenchymal proliferations (arrowhead), and (h) AFE with collagen-filled alveolar spaces and hyperelastosis of the remodeled alveolar septae (arrowhead). (D) Cinematic rendering of a hierarchical phase-contrast tomography scan from a 74-year-old male patient who succumbed to COVID-19 depicts the mosaic-like affection of lung parenchyma (left) as well as the spatial heterogeneity of affected airways in COVID-19 (right). AFE = alveolar fibroelastosis.
See this image and copyright information in PMC

Comment in

Comment on

  • Viral Infection, Pulmonary Fibrosis, and Long COVID.
    Hatabu H, Kaye KM, Christiani DC. Hatabu H, et al. Am J Respir Crit Care Med. 2023 Mar 15;207(6):647-649. doi: 10.1164/rccm.202211-2121ED. Am J Respir Crit Care Med. 2023. PMID: 36470237 Free PMC article. No abstract available.

References

    1. Hatabu H, Kaye KM, Christiani DC. Viral infection, pulmonary fibrosis, and long Covid. Am J Respir Crit Care Med . 2023;207:647–648. - PMC - PubMed
    1. Kamp JC, Neubert L, Ackermann M, Stark H, Werlein C, Fuge J, et al. Time-dependent molecular motifs of pulmonary fibrogenesis in COVID-19. Int J Mol Sci . 2022;23:1583. - PMC - PubMed
    1. Ackermann M, Kamp JC, Werlein C, Walsh CL, Stark H, Prade V, et al. The fatal trajectory of pulmonary COVID-19 is driven by lobular ischemia and fibrotic remodelling. EBioMedicine . 2022;85:104296. - PMC - PubMed
    1. Ackermann M, Stark H, Neubert L, Schubert S, Borchert P, Linz F, et al. Morphomolecular motifs of pulmonary neoangiogenesis in interstitial lung diseases. Eur Respir J . 2020;55:1900933. - PubMed
    1. Ackermann M, Verleden SE, Kuehnel M, Haverich A, Welte T, Laenger F, et al. Pulmonary vascular endothelialitis, thrombosis, and angiogenesis in Covid-19. N Engl J Med . 2020;383:120–128. - PMC - PubMed