Recognition of specific parts of microorganism is mediated by CRD in presence of calcium.[1][2] Affinity of interaction between microbes and collectins depends on the degree of collectin oligomerization and also on the density of ligands on the surface of the microbe.[3]
Collectins can bind to the surface of microorganisms and between carbohydrate ligands. Due to these properties, the interaction can result in aggregation.[5][6]
Opsonization and activation of phagocytosis
Collectins can act as opsonins. There is a specific interaction between collectins and receptors on phagocytic cells which can lead to increased clearance of microorganisms.[7][8][9] MBL can bind to microorganisms and this interaction can lead to opsonization through complement activation,[10] or it can opsonize the microorganism directly.[11] SP-A and SP-D can also interact with microorganisms and phagocytic cells to enhance phagocytosis of the microorganism.[12]
Inhibition of microbial growth
Collectins have effect on microorganism survival. SP-A and SP-D can bind to LPS (lipopolysaccharide) of both Gram-negative and Gram-positive bacteria. SP-A and SP-D can increase permeability of Gram-negative bacterial cell membrane.[13]
Modulation of inflammatory responses
SP-A and SP-D can damp induction of inflammation by LPS or endotoxin. It can be caused by removing the LPS or by binding the LPS to CD14 receptor on macrophages that can block the inflammatory response.[14][15][16] SP-A can also bind to TLR2 (toll-like receptor 2). This interaction causes decrease of TNF-α (tumor necrosis factor-α) production by alveolar macrophages stimulated with peptidoglycan.[17] SP-A and SP-D can modulate cytokine production. They modulate the production of oxygen and nitrogen reactive species which are very important for phagocytic cells.[18][19][20] SP-A and SP-D has s function as chemoattractants for alveolar neutrophils and monocytes.[21] MBL can recognize peptidoglycan via N-acetylglucosamine. This interaction leads to inhibition of ligand-induced inflammatory by macrophage chemokine production.[22]
Modulation of the adaptive immune system
SP-A and SP-D can suppress activated T-lymphocytes and IL-2 (interleukin-2) production.[23][24] SP-D increases bacterial antigen presentation by dendritic cells[25] whereas SP-A blocs differentation of the immature dendritic cells.[26]
Modulation of allergic response
Collectins SP-A and SP-D have anti-allergic effects: they inhibit IgE binding to allergens, decrease histamine release from basophils, and inhibit T-lymphocyte production in the late phase of the inflammation.[27][28][29]
Apoptosis
Collectins SP-A and SP-D enhance clearance of apoptotic cells by macrophages.[30][31]
Complement activation
Collectins are linked with activation of lectin pathway of complement activation. At the beginning, there is a binding of collectin to PAMPs or DAMPs. Collectin MBL is involved in activation of the lectin complement pathway.[32][33] There are three serine proteases, MASP-1, 2 and 3 (MBL-associated serine proteases), which participate in activation of the lectin pathway. MASP-2 has a cleavage activity and it is essential for forming lectin C3 and C5 convertases and for activation of the complement.[34][35][36]
Reviews
For more information and details see reviews:[37][38][39]
^McNeely, T B; J D Coonrod (July 1994). "Aggregation and opsonization of type A but not type B Hemophilus influenzae by surfactant protein A". American Journal of Respiratory Cell and Molecular Biology. 11 (1): 114–122. doi:10.1165/ajrcmb.11.1.8018334. ISSN1044-1549. PMID8018334.
^Hartshorn, K L; E Crouch; M R White; M L Colamussi; A Kakkanatt; B Tauber; V Shepherd; K N Sastry (June 1998). "Pulmonary surfactant proteins A and D enhance neutrophil uptake of bacteria". The American Journal of Physiology. 274 (6 Pt 1): L958–969. doi:10.1152/ajplung.1998.274.6.L958. ISSN0002-9513. PMID9609735.
^Borron, P; J C McIntosh; T R Korfhagen; J A Whitsett; J Taylor; J R Wright (April 2000). "Surfactant-associated protein A inhibits LPS-induced cytokine and nitric oxide production in vivo". American Journal of Physiology. Lung Cellular and Molecular Physiology. 278 (4): L840–847. doi:10.1152/ajplung.2000.278.4.l840. ISSN1040-0605. PMID10749762. S2CID25269338.
^Tino, M J; J R Wright (January 1999). "Surfactant proteins A and D specifically stimulate directed actin-based responses in alveolar macrophages". The American Journal of Physiology. 276 (1 Pt 1): L164–174. doi:10.1152/ajplung.1999.276.1.L164. ISSN0002-9513. PMID9887069.
^Borron, P; F X McCormack; B M Elhalwagi; Z C Chroneos; J F Lewis; S Zhu; J R Wright; V L Shepherd; F Possmayer; K Inchley; L J Fraher (October 1998). "Surfactant protein A inhibits T cell proliferation via its collagen-like tail and a 210-kDa receptor". The American Journal of Physiology. 275 (4 Pt 1): L679–686. doi:10.1152/ajplung.1998.275.4.L679. ISSN0002-9513. PMID9755099.
^Brinker, K G; E Martin; P Borron; E Mostaghel; C Doyle; C V Harding; J R Wright (December 2001). "Surfactant protein D enhances bacterial antigen presentation by bone marrow-derived dendritic cells". American Journal of Physiology. Lung Cellular and Molecular Physiology. 281 (6): L1453–1463. doi:10.1152/ajplung.2001.281.6.l1453. ISSN1040-0605. PMID11704542. S2CID1356964.
^Brinker, Karen G; Hollie Garner; Jo Rae Wright (January 2003). "Surfactant protein A modulates the differentiation of murine bone marrow-derived dendritic cells". American Journal of Physiology. Lung Cellular and Molecular Physiology. 284 (1): L232–241. doi:10.1152/ajplung.00187.2002. ISSN1040-0605. PMID12388334.
^Wang, J Y; C C Shieh; P F You; H Y Lei; K B Reid (August 1998). "Inhibitory effect of pulmonary surfactant proteins A and D on allergen-induced lymphocyte proliferation and histamine release in children with asthma". American Journal of Respiratory and Critical Care Medicine. 158 (2): 510–518. doi:10.1164/ajrccm.158.2.9709111. ISSN1073-449X. PMID9700129.
^Schwaeble, Wilhelm; Mads R Dahl; Steffen Thiel; Cordula Stover; Jens C Jensenius (September 2002). "The mannan-binding lectin-associated serine proteases (MASPs) and MAp19: four components of the lectin pathway activation complex encoded by two genes". Immunobiology. 205 (4–5): 455–466. doi:10.1078/0171-2985-00146. ISSN0171-2985. PMID12396007.
^Schwaeble, Wilhelm; Mads R Dahl; Steffen Thiel; Cordula Stover; Jens C Jensenius (September 2002). "The mannan-binding lectin-associated serine proteases (MASPs) and MAp19: four components of the lectin pathway activation complex encoded by two genes". Immunobiology. 205 (4–5): 455–466. doi:10.1078/0171-2985-00146. ISSN0171-2985. PMID12396007.
^Thiel, S; T Vorup-Jensen; C M Stover; W Schwaeble; S B Laursen; K Poulsen; A C Willis; P Eggleton; S Hansen; U Holmskov; K B Reid; J C Jensenius (1997-04-03). "A second serine protease associated with mannan-binding lectin that activates complement". Nature. 386 (6624): 506–510. Bibcode:1997Natur.386..506T. doi:10.1038/386506a0. ISSN0028-0836. PMID9087411. S2CID4261967.