title: Downregulation of Blood Monocyte HLA-DR in ICU Patients Is Also Present in Bone Marrow Cells.
abstract: BACKGROUND
  The downregulation of blood monocyte HLA-DR expression also occurs in tissue infiltrative cells in a context of acute clinical inflammation, especially sepsis. This context favors the development of secondary infections and results from various mechanisms. Little is known about HLA-DR expression on bone marrow (BM) cells of the monocyte lineage, the source of circulating monocytes. This study analyzed the BM HLA-DR expression in ICU patients compared to BM monocytes from non-ICU patients and to blood monocytes of control healthy donors. A potential dysfunction of myeloid differentiation was investigated in a sub-population of these ICU patients to characterize the phenotype of the immature forms of monocytes and granulocytes in BM.
  
  
  RESULTS
  BM and blood were drawn from 33 ICU and 9 non-ICU patients having a BM analysis to precise the etiology of abnormal low count in blood cells. The data were compared with blood cells of 28 control donors. Flow cytometry was used for both HLA-DR expression and phenotyping of immature forms of monocytes and granulocytes. HLA-DR expression was downregulated in both blood and BM monocyte in ICU patients compared to BM of non-ICU patients and blood of control donors. Amplitude of HLA-DR downregulation was comparable in septic and non-septic ICU patients. The phenotype of immature forms of monocytes and granulocytes in BM (n = 11) did not show abnormal myeloid (monocyte + granulocyte) differentiation.
  
  
  CONCLUSIONS
  The downregulation of HLA-DR in BM monocyte lineage is present in ICU patients without major changes in myeloid cells. It may result from a regulation mediated by soluble and/or neuro-endocrine factors present in BM cell microenvironment.
authors.affiliation: Inserm, U 1160, Paris, France.|University Paris Diderot, Sorbonne Paris Cité, Paris, France.
authors.forename: Valérie
authors.initials: V
authors.lastname: Faivre
authors.affiliation: Inserm, U 1160, Paris, France.|University Paris Diderot, Sorbonne Paris Cité, Paris, France.|AP-HP, Hôpital Lariboisière, Département d'Anesthésie - Réanimation - SMUR, Paris, France.
authors.forename: Anne-Claire
authors.initials: AC
authors.lastname: Lukaszewicz
authors.affiliation: Inserm, U 1160, Paris, France.|University Paris Diderot, Sorbonne Paris Cité, Paris, France.|AP-HP, Hôpital Lariboisière, Département d'Anesthésie - Réanimation - SMUR, Paris, France.
authors.forename: Didier
authors.initials: D
authors.lastname: Payen
mesh_terms: D000368:Aged; D001854:Bone Marrow Cells / Q000378:metabolism*; D039481:CD11b Antigen / Q000097:blood / Q000378:metabolism; D016022:Case-Control Studies; D015536:Down-Regulation; D005260:Female; D058851:GPI-Linked Proteins / Q000097:blood / Q000378:metabolism; D006684:HLA-DR Antigens / Q000097:blood / Q000378:metabolism*; D006801:Humans; D007362:Intensive Care Units; D019041:L-Selectin / Q000097:blood / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism* / Q000473:pathology; D011446:Prospective Studies; D054390:Receptors, CCR2 / Q000097:blood / Q000378:metabolism; D017452:Receptors, IgG / Q000097:blood / Q000378:metabolism; D012772:Shock, Septic / Q000097:blood / Q000378:metabolism; D013921:Thrombocytopenia / Q000097:blood / Q000378:metabolism
chemical_list: C515334:CCR2 protein, human; D039481:CD11b Antigen; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D006684:HLA-DR Antigens; C509295:ITGAM protein, human; D054390:Receptors, CCR2; D017452:Receptors, IgG; D019041:L-Selectin