PMID- 15793118
OWN - NLM
STAT- MEDLINE
DCOM- 20050512
LR  - 20181113
IS  - 0066-4804 (Print)
IS  - 1098-6596 (Electronic)
IS  - 0066-4804 (Linking)
VI  - 49
IP  - 4
DP  - 2005 Apr
TI  - Differential expression of cytokines and chemokines in human monocytes induced by 
      lipid formulations of amphotericin B.
PG  - 1397-403
AB  - The immunomodulatory effects of liposomal amphotericin B (LAMB), amphotericin B 
      lipid complex (ABLC), and amphotericin B colloidal dispersion (ABCD) on mRNA and 
      protein profiles of five cytokines and chemokines expressed by human 
      monocyte-enriched mononuclear leukocytes (MNCs) were comprehensively evaluated by 
      semiquantitative reverse transcription-PCR and enzyme-linked immunosorbent 
      assays; they were compared to those of deoxycholate amphotericin B (DAMB). mRNAs 
      of interleukin-1beta (IL-1beta), IL-1 receptor antagonist (IL-1ra), tumor 
      necrosis factor alpha (TNF-alpha), monocyte chemotactic protein 1 (MCP-1), and 
      macrophage inflammatory protein 1beta (MIP-1beta) were assessed after treatment 
      of MNCs with each drug for 0.5, 2, 6, and 22 h. The cytokine protein profiles 
      were obtained after incubation of MNCs with the drugs for 2 h (TNF-alpha) or 6 h 
      (all the others). In the mRNA studies, DAMB resulted in an early increase of 
      inflammatory cytokines or chemokines IL-1beta, TNF-alpha, MCP-1, and MIP-1beta (2 
      to 6 h) and in a late increase of anti-inflammatory IL-1ra (22 h). ABCD showed a 
      general similar trend of inflammatory gene up-regulation. LAMB and ABLC decreased 
      or did not affect IL-1beta and TNF-alpha, whereas ABLC additionally decreased 
      MIP-1beta. In protein measurement studies, DAMB and ABCD up-regulated production 
      of IL-1beta (P < 0.05), decreased the IL-1ra/IL-1beta ratio, and up-regulated the 
      production of MCP-1 and MIP-1beta. In comparison, LAMB and ABLC down-regulated or 
      did not affect the production of these cytokines/chemokines compared to untreated 
      MNCs; furthermore, ABLC tended to increase the IL-1ra/IL-1beta ratio. These 
      studies demonstrate that amphotericin B formulations differentially affect gene 
      expression and release of an array of proinflammatory and anti-inflammatory 
      cytokines that potentially may explain the differences in infusion-related 
      reactions and dose-dependent nephrotoxicity as well as modulation of the host 
      immune response to invasive fungal infections.
FAU - Simitsopoulou, M
AU  - Simitsopoulou M
AD  - Laboratory of Infectious Diseases, 3rd Department of Pediatrics, School of 
      Medicine, Aristotle University of Thessaloniki, Greece.
FAU - Roilides, E
AU  - Roilides E
FAU - Dotis, J
AU  - Dotis J
FAU - Dalakiouridou, M
AU  - Dalakiouridou M
FAU - Dudkova, F
AU  - Dudkova F
FAU - Andreadou, E
AU  - Andreadou E
FAU - Walsh, T J
AU  - Walsh TJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Antimicrob Agents Chemother
JT  - Antimicrobial agents and chemotherapy
JID - 0315061
RN  - 0 (Antifungal Agents)
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (Liposomes)
RN  - 0 (RNA, Messenger)
RN  - 005990WHZZ (Deoxycholic Acid)
RN  - 7XU7A7DROE (Amphotericin B)
SB  - IM
MH  - Amphotericin B/chemistry/*pharmacology
MH  - Antifungal Agents/chemistry/*pharmacology
MH  - Chemistry, Pharmaceutical/methods
MH  - Chemokines/genetics/metabolism
MH  - Cytokines/genetics/*immunology/*metabolism
MH  - Deoxycholic Acid
MH  - Gene Expression Regulation
MH  - Humans
MH  - Liposomes
MH  - Monocytes/*immunology/metabolism
MH  - RNA, Messenger/genetics/metabolism
PMC - PMC1068615
EDAT- 2005/03/29 09:00
MHDA- 2005/05/13 09:00
PMCR- 2005/04/01
CRDT- 2005/03/29 09:00
PHST- 2005/03/29 09:00 [pubmed]
PHST- 2005/05/13 09:00 [medline]
PHST- 2005/03/29 09:00 [entrez]
PHST- 2005/04/01 00:00 [pmc-release]
AID - 49/4/1397 [pii]
AID - 0960-04 [pii]
AID - 10.1128/AAC.49.4.1397-1403.2005 [doi]
PST - ppublish
SO  - Antimicrob Agents Chemother. 2005 Apr;49(4):1397-403. doi: 
      10.1128/AAC.49.4.1397-1403.2005.