Disease relevance of CCL7

• TAQMAN, immunohistochemical, and ELISA analyses confirmed that CCL7 was expressed at significantly higher levels in UIP lung biopsies compared with biopsies from patients with nonspecific interstitial pneumonia, respiratory bronchiolitis-interstitial lung disease, and from patients without IIP [1].
• Together, these data suggest that CCL7 is highly expressed in biopsies and pulmonary fibroblast lines obtained from patients with UIP relative to patients with other IIP and patients without IIP, and that this CC chemokine may have a major role in the progression of fibrosis in this IIP patient group [1].
• MCP-1-MCP-3-Eotaxin gene cluster influences HIV-1 transmission [2].
• Whole mycobacteria (Mycobacterium bovis BCG) strongly induced MCP-3 expression [3].
• MCP-3 (CCL7) delivered by parvovirus MVMp reduces tumorigenicity of mouse melanoma cells through activation of T lymphocytes and NK cells [4].

Psychiatry related information on CCL7

• The discussion is by Marc Schuckit, who was chair of the Substance Use disorders (SUD) Committee for DSM-IV and cochair of the international group of experts reviewing the SUD definitions for DSM-V [5].
• He not only sent the 1836 memoir of Marc Dax, his deceased father, to Paris in 1863, but saw to it that this important document was published before Paul Broca's own article on cerebral dominance appeared later in 1865 [6].
• Alzheimer's disease: how research is changing primary care management. Interview by Marc E. Weksler [7].

High impact information on CCL7

• Inflammation dampened by gelatinase A cleavage of monocyte chemoattractant protein-3 [8].
• Cleaved MCP-3 binds to CC-chemokine receptors-1, -2, and -3, but no longer induces calcium fluxes or promotes chemotaxis, and instead acts as a general chemokine antagonist that dampens inflammation [8].
• On these cells, it binds to receptors that recognize MCP-1, MCP-3, and RANTES [9].
• On eosinophils, MCP-4 has similar efficacy and potency as MCP-3, RANTES, and cotaxin [9].
• Like MCP-3, MCP-4 is a chemoattractant of high efficacy for monocytes and T lymphocytes [9].

Chemical compound and disease context of CCL7

• In combination with aminoglycoside antibiotics, temocillin exerted a synergistic or partially synergistic effect (sigma FIC less than or equal to 0.75) against the majority of strains of Pseudomonas aeruginosa tested [10].
• MCP-3 levels correlated positively with the extent of skin fibrosis, and inversely with %VC and carbon monoxide transfer factor (Tlco) in patients with SSc [11].
• The in-vitro activity of clarithromycin, temafloxacin, and ethambutol were assessed by MIC, FIC and intra-macrophage killing determinations alone and in various combinations against ten pigmented and ten non-pigmented strains of Mycobacterium avium complex bacteria [12].
• The effect of beta-cryptoxanthin, a kind of carotenoid, on ovariectomy-induced bone loss was investigated. beta-cryptoxanthin was isolated from Satsuma mandarin (Citrus unshu. MARC). beta-cryptoxanthin (5 or 10 microg/100 g body weight) was orally administered once daily for 3 months to ovariectomized (OVX) rats [13].
• Evaluation of in vitro interaction of daptomycin with gentamicin or beta-lactam antibiotics against Staphylococcus aureus and Enterococci by FIC index and timed-kill curves [14].

Biological context of CCL7

• By gene array analysis, upper and lower lobe biopsies and primary fibroblast lines from patients with usual interstitial pneumonia (UIP), nonspecific interstitial pneumonia, and respiratory bronchiolitis-interstitial lung disease, but not patients without IIP, exhibited CCL7 gene expression [1].
• They also induced the release of histamine and leukotrienes in IL-3-primed basophils, but their efficacy was lower than that of MCP-1 and MCP-3, which were the most potent stimuli of exocytosis [15].
• In order to isolate receptor(s) for MCP3, a cDNA library was constructed using mRNA from a human NK-like cell line, YT [16].
• These cells showed high affinity binding sites for 125I-MCP3 and migrated in response to MCP3 [16].
• In the chemotaxis assay under agarose, MCP-3 dose-dependently increased the migration distance of neutrophils toward IL-8 [17].

Anatomical context of CCL7

• In eosinophils, by contrast, cross-desensitization between RANTES and MCP-3 was obtained [18].
• Thus, MCP-3 was as effective as MCP-1 as an inducer of mediator release, and as effective as RANTES as a stimulus of basophil migration [18].
• MCP-1, MCP-2, and MCP-3 are potent chemoattractants for monocytes, basophils, and T lymphocytes [19].
• MCP3 has been reported to interact with several C-C chemokine receptors, which can be simultaneously or selectively expressed on leukocyte subpopulations [16].
• The purpose of this study is to establish how MCP3 binds and activates monocytes and neutrophils [20].

Associations of CCL7 with chemical compounds

• We have isolated a cDNA (NC28) transcribed from a mRNA which is transiently induced in U937 promonocytic cells by PMA and super-induced by cycloheximide [21].
• Pretreatment with actinomycin D abolished LAM-induced MCP-3 expression, whereas cycloheximide only partially reduced the expression [3].
• MCP-1 and MCP-3 rapidly induced arachidonic acid release whereas MCP-2 was ineffective [22].
• Furthermore, the dissociation constant between MCP-3 and Arixtra was determined by using electrospray ionization Fourier transform ion cyclotron resonance (ESI FT-ICR) mass spectrometry, which compared favorably with the result of the isothermal titration calorimetry (ITC) assay [23].
• This allowed the detection of a change in intracellular Ca(2+) after treatment with CCL7 and Met-RANTES showing that these ligands possess measurable but low efficacy [24].

Physical interactions of CCL7

• The transfectants (YT4/293) showed high affinity binding for 125I-MCP3 in addition to specifically binding 125I-MIP1 alpha and 125I-Rantes [16].
• RANTES and MCP-3 antagonists bind multiple chemokine receptors [25].

Regulatory relationships of CCL7

• MCP-3 bound to HEK-293 cells stably expressing the MCP-1 receptor, but with approximately 35-fold lower affinity than MCP-1 [19].
• Monocyte chemotactic protein 3 is a most effective basophil- and eosinophil-activating chemokine [18].
• The phenotype frequency (PF) of none of the MCP-3 alleles was significantly altered in the population of controls versus unselected MS patients [26].
• Interferon-beta (IFN-beta) induced MCP-3 mRNA after 16 hr, a time point when the PMA-induced mRNA had the tendency to level off [27].

Other interactions of CCL7

• MCP3, MIP1 alpha, and Rantes were equally able to cross-attenuate the migratory response of YT4/293 cells to one another [16].
• In this study, we have examined potential interactions of MCP-2 and MCP-3 with the recently cloned MCP-1 receptor [19].
• In contrast, responses to MCP-3 were blocked only in the presence of both mAbs, but not after pretreatment with either anti-CCR2 or anti-CCR3 mAb alone [28].
• MCP3 in our study was also the only human CC chemokine that consistently chemoattracted neutrophils [20].
• Bacteria-induced CCL2, CCL7, CXCL9, and CXCL10 mRNA expression was partially dependent on ongoing protein synthesis [29].

Analytical, diagnostic and therapeutic context of CCL7

• We now provide evidence that current immunosuppression protocols have a limited effect on monocyte inflammatory cytokine production and do not adequately suppress monocyte IL-8, MCP-1, and MCP-3 chemokine production [30].
• The full-length cDNA revealed an open reading frame for a 98-amino acid residue protein, and a sequence alignment with known CC chemokines showed high levels of similarity (59-62%) with MCP-1, MCP-3, and eotaxin [31].
• The relative binding affinity of these ligands to MCP-3 was also determined using a competitive filtration trapping assay [23].
• Human monocyte chemotactic protein-3 (MCP-3): molecular cloning of the cDNA and comparison with other chemokines [32].
• Tissue was processed for immunocytochemistry (ICC) and for in situ hybridization using 35S-labeled riboprobes for RANTES and MCP-3 [33].

References